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Post-acute myocardial infarction (AMI) fibrosis is a pathophysiologic process characterised by activation of the profibrotic mediator, transforming growth factor-ß (TGF-ß). AMI is associated with a substantial increase in the levels of extracellular adenosine triphosphate (eATP), which acts on the purinergic P2X7-receptor (P2X7-R) and triggers an inflammatory response that contributes to myocardial fibrotic remodelling. P2X7-R has been implicated in several cardiovascular diseases; however, its role in the regulation of cardiac fibrosis remains unclear. Therefore, the current study aimed to determine the effect of the P2X7-R antagonist, A740003, on post-AMI fibrosis, via the profibrotic TGF-ß1/Smad signalling pathway, and elucidate whether its effect is mediated via the modulation of GSK-3ß. AMI was induced by surgical ligation of the left anterior descending coronary artery, Thereafter, animals were divided into groups: sham control, MI-untreated, MI-vehicle, and MI-A740003 (50 mg/kg/day) and treated for seven days accordingly. The heart weight/body weight ratio of untreated-ligated rats significantly increased by 15.1 %, creatine kinase-MB (CK-MB) significantly increased by 40 %, troponin-I levels significantly increased by 25.4 %, and lactate dehydrogenase significantly increased by 47.2 %, indicating myocardial damage confirmed by morphological changes and massive cardiac fibrosis. The protein expression of cardiac fibronectin, TGF-ß1, and p-Smad2 were also upregulated by 143 %, 40 %, and 8 %, respectively, indicating cardiac fibrosis. The treatment of ligated rats with A740003 led to improvement in all the above-mentioned parameters. Overall, A740003 exhibits potential cardio-protective effects on post-AMI fibrotic remodelling in the animal model of AMI through P2X7-R blockade, possibly by downregulating the profibrotic TGF-ß1/Smad signalling pathway and restoring GSK-3ß phosphorylation. Altogether, treatment with A740003 could serve as a new cardioprotective strategy to attenuate post-AMI fibrotic remodelling.

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Type 2 diabetes mellitus (T2DM) is a critical health problem, with 700 million diagnoses expected worldwide by 2045. Uncontrolled high blood glucose levels can lead to serious complications, including diabetic cardiomyopathy (DCM). Diabetes induces cardiovascular aging and inflammation, increasing cardiomyopathy risk. DCM is characterized by structural and functional abnormalities in the heart. Growing evidence suggests that cellular senescence and macrophage-mediated inflammation participate in the pathogenesis and progression of DCM. Evidence indicates that growth differentiation factor-15 (GDF-15), a protein that belongs to the transforming growth factor-beta (TGF-ß) superfamily, is associated with age-related diseases and exerts an anti-inflammatory role in various disease models. Although further evidence suggests that GDF-15 can preserve Klotho, a transmembrane antiaging protein, emerging research has elucidated the potential involvement of GDF-15 and Klotho in the interplay between macrophages-induced inflammation and cellular senescence in the context of DCM. This review explores the intricate relationship between senescence and macrophages in DCM while highlighting the possible contributions of GDF-15 and Klotho.

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One of the possible candidates for the treatment of diabetic cardiomyopathy is liraglutide, a glucagon-like peptide-1 receptor (GLP1R) agonist. In this study, the impacts of liraglutide on the integrin-linked kinase (ILK)-related PI3K/AKT axis in rats with type 2 diabetes induced via streptozotocin were examined. Twenty-four Wistar albino rats were distributed in four different groups, and a high-fat diet and streptozotocin were used to induce type 2 in two groups. Rats in the untreated control groups were administered 0.9% NaCl solution over a 6-week period, and those in the treatment groups were administered 0.9% NaCl for 3 weeks, followed by subcutaneous injection of liraglutide (150 µg/kg) for an additional 3 weeks. In the liraglutide-treated diabetic group, the heart-to-body weight ratio was significantly reduced, levels of cardiac biomarkers, troponin I and creatine-kinase-MB, were improved; activities of antioxidant enzymes, glutathione peroxidase and superoxide dismutase, were increased; and levels of malondialdehyde were decreased. Western blotting and immunohistochemical studies revealed increased levels of ILK, P-PI3K, P-AKT, and BCL2, as well as those of caspase 3, BAX, and P-PTEN, indicating mitigation of cardiomyocyte apoptosis. Our results show that liraglutide, by targeting GLP1Rs, enhances the expression of proteins in the ILK/PI3K/AKT/PTEN pathway and thereby exerts its cardioprotective effects in rats with DCM.

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OBJECTIVES: Diabetic cardiomyopathy is a known complication of diabetes mellitus. Herein, we aimed to determine whether glycemic control mediated by sitagliptin, a dipeptidyl peptidase-4 inhibitor, can ameliorate diabetic myocardial abnormalities by modulating TGF-ß signaling via the SMAD and integrin-linked kinase (ILK) pathways. METHODS: Four groups of male Wistar albino rats were used, with six rats in each group. Two nondiabetic and two diabetic (produced by a single intraperitoneal dose of streptozotocin (55 mg/kg)) groups were administered either normal saline or sitagliptin (100 mg/kg) orally for 6 weeks. Subsequently, HW/BW ratios and cardiac enzymes were assessed, along with a histological examination of cardiac tissues. Levels of TGF-ß, collagen I, p-SMAD2/3, TNF-α, MMP-9, and ILK were detected. RESULTS: Compared with the diabetic control group, sitagliptin-treated diabetic rats exhibited considerably reduced HW/BW ratios and troponin I and creatine kinase-MB levels, with improvements in histopathological changes in cardiac tissues. TGF-ß, collagen I, p-SMAD2/3, TNF-α, and MMP-9 levels were significantly decreased in the sitagliptin-treated diabetic group, whereas ILK was elevated following sitagliptin treatment. CONCLUSION: Sitagliptin could afford cardioprotective effects for the first time by altering ILK-associated TGF-ß/SMAD signaling pathways. Thus, sitagliptin may be a promising therapeutic target for the prevention of diabetic cardiomyopathy.

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Pathological cardiac remodeling is associated with cardiovascular disease and can lead to heart failure. Nuclear factor-kappa B (NF-κB) is upregulated in the hypertrophic heart. Moreover, the expression of the G-protein-coupled receptor kinase 2 (GRK2) is increased and linked to the progression of heart failure. The inhibitory effects of paroxetine on GRK2 have been established. However, its protective effect on IκBα/NFκB signaling has not been elucidated. This study investigated the cardioprotective effect of paroxetine in an animal model of cardiac hypertrophy (CH), focusing on its effect on GRK2-mediated NF-κB-regulated expression of prohypertrophic and profibrotic genes. Wistar albino rats were administered normal saline, paroxetine, or fluoxetine, followed by isoproterenol to induce CH. The cardioprotective effects of the treatments were determined by assessing cardiac injury, inflammatory biomarker levels, histopathological changes, and hypertrophic and fibrotic genes in cardiomyocytes. Paroxetine pre-treatment significantly decreased the HW/BW ratio (p < 0.001), and the expression of prohypertrophic and profibrotic genes Troponin-I (p < 0.001), BNP (p < 0.01), ANP (p < 0.001), hydroxyproline (p < 0.05), TGF-ß1 (p < 0.05), and αSMA (p < 0.01) as well as inflammatory markers. It also markedly decreased pIκBα, NFκB(p105) subunit expression (p < 0.05) and phosphorylation. The findings suggest that paroxetine prevents pathological cardiac remodeling by inhibiting the GRK2-mediated IκBα/NF-κB signaling pathway.

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Prolonged vasoconstrictor signalling found in hypertension, increases arterial contraction, and alters vessel architecture by stimulating arterial smooth muscle cell (ASMC) growth, underpinning the development of re-stenosis lesions and vascular remodelling. Vasoconstrictors interact with their cognate G protein coupled receptors activating a variety of signalling pathways to promote smooth muscle proliferation. Here, angiotensin II (AngII) and endothelin 1 (ET1), but not UTP stimulates ASMC proliferation. Moreover, siRNA-mediated depletion of endogenous GRK2 expression, or GRK2 inhibitors, compound 101 or paroxetine, prevented AngII and ET1-promoted ASMC growth. Depletion of GRK2 expression or inhibition of GRK2 activity ablated the prolonged phase of AngII and ET-stimulated ERK signalling, while enhancing and prolonging UTP-stimulated ERK signalling. Increased GRK2 expression enhanced and prolonged AngII and ET1-stimulated ERK signalling, but suppressed UTP-stimulated ERK signalling. In ASMC prepared from 6-week-old WKY and SHR, AngII and ET1-stimulated proliferation rates were similar, however, in cultures prepared from 12-week-old rats AngII and ET1-stimulated growth was enhanced in SHR-derived ASMC, which was reversed following depletion of GRK2 expression. Furthermore, in ASMC cultures isolated from 6-week-old WKY and SHR rats, AngII and ET1-stimulated ERK signals were similar, while in cultures from 12-week-old rats ERK signals were both enhanced and prolonged in SHR-derived ASMC, and were reversed to those seen in age-matched WKY-derived ASMC following pre-treatment of SHR-derived ASMC with compound 101. These data indicate that the presence of GRK2 and its catalytic activity are essential to enable pro-proliferative vasoconstrictors to promote growth via recruitment and activation of the ERK signalling pathway in ASMC.

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Background and Objectives: Physical activity is essential for adolescents to maintain a healthy lifestyle. The aim of this study was to assess the influence of an 8-week exercise program and motivation on physical activity levels, self-motivation, and mental well-being of adolescents in Saudi Arabia. Moreover, the impact of virtual coaching on physical, emotional, and mental health after an eight-week exercise program was examined. Materials and Methods: Twenty-seven participants, 18 females (67%) and 9 males (33%), with a mean age of 14 ± 2.38 years, were enrolled in eight weeks of pre- and post-intervention between June and August of 2021. The physical activity scale, situational motivation scale, mental health continuum short form, and baseline assessments were completed before and after the eight-week program. The program recommended that adolescents practice aerobic, resistance, and weight-bearing exercises for 60 min daily. Paired mean t-tests were used to compare pre-and post-test results. Results: Participants showed an acceptable physical activity level (5.5 ± 1.4) on a 10-point scale with a significant improvement after the eight-week program (7 ± 1.5; p = 0.013). The situational motivation scale improved from 38.1 ± 16 to 26 ± 19.6 (p = 0.042). The mental health continuum (social and psychological well-being) also significantly improved. Participants who received weekly phone calls showed similar improvement patterns but were not significantly different from those who did not receive calls. Conclusions: A virtually delivered 8-week exercise program for adolescents improved their physical, motivational, and mental health. Providing additional weekly phone calls does not provide additional improvement. Providing adolescents with the needed supervision and motivation enhances their physical activity and mental health.

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Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus. This study examined the therapeutic effects of sitagliptin, a dipeptidyl peptidase inhibitor, on DN and explored the underlying mechanism. Male Wistar albino rats (n = 12) were intraperitoneally administered a single dose of streptozotocin (30 mg/kg) to induce diabetes. Streptozotocin-treated and untreated rats (n = 12) were further divided into normal control, normal sitagliptin-treated control, diabetic control, and sitagliptin-treated diabetic groups (n = 6 in each). The normal and diabetic control groups received normal saline, whereas the sitagliptin-treated control and diabetic groups received sitagliptin (100 mg/kg, p.o.). We assessed the serum levels of DN and inflammatory biomarkers. Protein tyrosine phosphatase 1 B (PTP1B), phosphorylated Janus kinase 2 (P-JAK2), and phosphorylated signal transducer activator of transcription (P-STAT3) levels in kidney tissues were assessed using Western blotting, and kidney sections were examined histologically. Sitagliptin reduced DN and inflammatory biomarkers and the expression of PTP1B, p-JAK2, and p-STAT3 (p < 0.001) and improved streptozotocin-induced histological changes in the kidney. These results demonstrate that sitagliptin ameliorates inflammation by inhibiting DPP-4 and consequently modulating the PTP1B-related JAK/STAT axis, leading to the alleviation of DN.

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BACKGROUND: Myocardial infarction (MI) is considered a public health problem. According to the World Health Organization, MI is a leading cause of death and comorbidities worldwide. Activation of the α1A adrenergic receptor is a contributing factor to the development of MI. Tamsulosin, an α1A adrenergic blocker, has gained wide popularity as a medication for the treatment of benign prostatic hyperplasia. Limited evidence from previous studies has revealed the potential cardioprotective effects of tamsulosin, as its inhibitory effect on the α1A adrenoceptor protects the heart by acting on the smooth muscle of blood vessels, which results in hypotension; however, its effect on the infarcted heart is still unclear. The mechanisms of the expected cardioprotective effects mediated by tamsulosin are not yet understood. Transforming growth factor-beta (TGF-ß), a mediator of fibrosis, is considered an attractive therapeutic target for remodeling after MI. The role of α1A adrenoceptor inhibition or its relationships with integrin-linked kinase (ILK) and TGF-ß/small mothers against decapentaplegic (Smad) signaling pathways in attenuating MI are unclear. The present study was designed to investigate whether tamsulosin attenuates MI by modulating an ILK-related TGF-ß/Smad pathway. METHODS: Twenty-four adult male Wistar rats were randomly divided into 4 groups: control, ISO, TAM, and ISO + TAM. ISO (150 mg/kg, intraperitoneally) was injected on Days 20 and 21 to induce MI. Tamsulosin (0.8 mg/kg, orally) was administered for 21 days, prior to ISO injection for 2 consecutive days. Heart-to-body weight ratios and cardiac and fibrotic biomarker levels were subsequently determined. ILK, TGF-ß1, p-Smad2/3, and collagen III protein expression levels were determined using biomolecular methods. RESULTS: Tamsulosin significantly attenuated the relative heart-to-body weight index (p < 0.5) and creatine kinase-MB level (p < 0.01) compared with those in the ISO control group. While ISO resulted in superoxide anion production and enhanced oxidative damage, tamsulosin significantly prevented this damage through antioxidant defense mechanisms, increasing glutathione and superoxide dismutase levels (p < 0.05) and decreasing lipid peroxide oxidation levels (p < 0.01). The present data revealed that tamsulosin reduced TGF-ß/p-Smad2/3 expression and enhanced ILK expression. CONCLUSION: Tamsulosin may exert a cardioprotective effect by modulating the ILK-related TGF-ß/Smad signaling pathway. Thus, tamsulosin may be a useful therapeutic approach for preventing MI.

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BACKGROUND: The shortening of the pectoralis minor muscle (PMi-M) and weakening of the lower trapezius muscle (LTr-M) affect scapular movement, resulting in the development of a rounded shoulder posture and reduction in the shoulder flexion range of motion (SFROM). OBJECTIVE: This study evaluated the combined effect of LTr-M strengthening and PMi-M stretching on correcting the rounded shoulder postures and SFROM among young Saudi females. METHODS: This study was based on a two-arm parallel-group repeated measures randomized comparative design. A total of sixty female participants with rounded shoulder postures were recruited and randomly allocated into groups 1 and 2 (n = 30/group). Each group performed supervised PMi-M stretching; however, group 2 performed a combination of LTr-M strengthening and PMi-M stretching. The outcomes, including rounded shoulder posture and SFROM, were assessed using the pectoralis minor length test (PMLT) and universal goniometer. A repeated measure ANOVA was used to compare the differences within-group and between-group for the outcomes measures at one-week (baseline) pre-intervention, two weeks, and three -weeks post-intervention. The significance level was set at q > 2.00 and p < 0.05 for all respective statistical analyses. RESULTS: The within-group comparison revealed significant improvements (q > 2.00) in the outcomes of PMLT and SFROM when comparing their post-intervention scores to the baseline scores. The between-group comparison revealed a significant and an insignificant (q < 2.00) difference in the outcomes of PMLT and SFROM, respectively when comparing their scores at the second- and third-week post-intervention. Furthermore, the effect size of the intervention suggests an advantage of group 2 over group 1 in increasing the resting length of the PMi-M only among young Saudi females. CONCLUSIONS: The combined effect of LTr-M strengthening and PMi-M stretching was more beneficial than PMi-M stretching alone in correcting the rounded shoulder posture among young Saudi females by increasing PMi-M resting length. However, it could not yield a differential improvement in the SFROM outcome among them.

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The P2X7 purinergic receptor (P2X7R) is a non­selective cation channel activated by high levels of adenosine triphosphate that are commonly present in serious conditions. Activation of this purinergic receptor is closely related to the development of various disease states including inflammatory and neurodegenerative disorders, orthopedic diseases and types of cancer. Accumulating evidence has shown that the P2X7R plays a crucial role in the development of various heart diseases. For example, activation of P2X7Rs may alleviate myocardial ischemia­reperfusion injury by releasing endogenous cardiac protective substances. In contrast to these findings, activation of P2X7Rs can promote the development of acute myocardial infarction and myocarditis by inducing inflammatory responses. Activation of these receptors can also contribute to the development of different types of cardiomyopathies including diabetic cardiomyopathy, dilated cardiomyopathy and hypertrophic cardiomyopathy by inducing cardiac hypertrophy, fibrosis and apoptosis. Notably, inhibition of P2X7Rs can improve cardiac structure and function abnormalities following acute myocardial infarction, reduction of inflammatory responses following myocarditis and attenuation of the cardiomyopathy process. Furthermore, recent evidence has demonstrated that P2X7Rs are highly active in patients infected with coronavirus disease­2019 (COVID­19). Hyperactivation of P2X7Rs in COVID­19 may induce severe myocardial injury through the activation of several signaling pathways. The present study reviewed the important role of the P2X7R in cardiac dysfunctions and discusses its use as a possible new therapeutic approach for the prevention and treatment of several myocardial diseases.

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The aim of this study was to investigate the relationship between treatment-resistant depression (TRD) and inflammation in humans and experimental models. For the human study, a retrospective cohort study was conducted with 206 participants; half were on antidepressants for major depressive disorder. The patients were divided into healthy and depressed groups. Inflammation was assessed based on the values of the main inflammatory biomarkers (CRP, WBC and ESR). For the animal experiments, 35 adult male Wistar rats were assigned to stressed and non-stressed groups. Inflammation and stress were induced using lipopolysaccharide and chronic unpredictable mild stress. A 10 mg/kg intraperitoneal injection of fluoxetine (FLX), a known antidepressant, was simultaneously administered daily for 4 weeks. Behavioral tests were performed. The plasma levels of inflammatory and stress biomarkers were measured and were significantly higher in the stressed and non-responsive groups in both studies. This study provides evidence of the link between inflammation and TRD. We further observed a possible link via the Phosphorylated Janus Kinase 2 and Phosphorylated Signal Transducer and Activator of Transcription 3 (P-JAK2/P-STAT3) signaling pathway and found that chronic stress and high inflammation hinder the antidepressant effects of FLX. Thus, non-response to antidepressants could be mitigated by treating inflammation to improve the antidepressant effect in patients with TRD.

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Background: The severity of the articular lesion is the single most essential element in investigating the extent of flexion that is required for activities. However, a prior study found no differences in muscle strength gains of quadriceps muscles at different knee angles in people with patellofemoral pain syndrome (PFPS). Objective: The effects of patellar taping and electromyographic biofeedback (EMG-BF)-guided isometric quadriceps strengthening at different knee angles (e.g., 30°, 60°, and 90° of knee flexion) on quadriceps strength and functional performance in people with PFPS were compared in this single-blind randomized controlled parallel trial. Methods: Sixty adult male athletes with PFPS (age: 26.9 ± 1.4 years) were randomly divided into two groups. The experimental group (n = 30) received patellar taping and EMG-BF-guided isometric contraction exercise at 30°, 60°, and 90° angles, and the control group (n = 30) received sham patellar taping without EMG-BF-guided exercises for six weeks. Pain intensity, knee function, muscle strength, and the single-leg triple hop (SLTH) test were assessed. Results: The pain intensity and SLTH scores between the groups were significantly different at the end of the trial (p ≤ 0.001). The EMG-BF and control groups had mean pain scores of 1.3 (0.8) and 4.5 (0.8), respectively. The EMG-BF and control groups had mean functional scores of 80.4 (5.1) and 69.1 (6.1), respectively. The mean SLTH score for the EMG-BF group was 540.7 (51.2) and for the control group it was 509.4 (49.8) after the trial. Quadriceps muscle strength was significantly higher in those who performed quadriceps strength training at 60° of knee flexion after six weeks than in those who performed strength training at 30° or 90° of knee flexion. Conclusion: The findings indicated that individuals who trained their quadriceps at a 60° knee angle had significantly stronger quadriceps muscles than individuals who trained at 30° or 90° of knee flexion. Trial Registration. This trial is registered at Clinical Trials.gov under the identifier NCT05055284.

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Background: The study's objective was to analyze the influence of an 8-week neuromuscular electrical stimulation (NMES) with a plyometric (PT) and strength training (ST) program on muscular, sprint, and functional performances in collegiate male football players. Methods: Sixty collegiate male football players participated in this randomized controlled trial single-blind study. All the participants were randomly divided into two groups: (1) NMES group (Experimental, n = 30) who received NMES assisted ST and (2) sham NMES group (Control, n = 30) who received sham NMES assisted ST. In addition, participants from both groups received a PT program; both groups received intervention on three days a week for 8-weeks. The study's outcomes, such as muscular, sprint, and functional performances, were assessed using a strength test (STN) for quadriceps muscle, sprint test (ST), and single-leg triple hop test (SLTHT), respectively, at baseline pre-intervention and 8-week post-intervention. The interaction between group and time was identified using a mixed design (2 × 2) ANOVA. Results: Significant difference found across the two time points for the scores of STN: F (1.58) = 5,479.70, p < 0.05; SLTHT: F (1.58) = 118.17, p < 0.05; and ST: F (1.58) = 201.63, p < 0.05. Similarly, the significant differences were found between groups averaged across time for the scores of STN: F (1.58) = 759.62, p < 0.05 and ST: F (1.58) = 10.08, p < 0.05. In addition, after 8-week of training, Cohen's d observed between two groups a large to medium treatment's effect size for the outcome STN (d = 10.84) and ST (d = 1.31). However, a small effect size was observed only for the SLTHT (d = 0.613). Conclusions: Findings suggest that the effect of PT and ST with either NMES or sham NMES are equally capable of enhancing muscular, sprint, and functional performances in collegiate male football players. However, PT and ST with NMES have shown an advantage over PT and ST with sham NMES in improving muscular performance and sprint performance among the same participants.

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Conducted during the second wave of the pandemic, this cross-sectional study examined the link between sleep quality, physical activity, exposure, and the impact of COVID-19 as predictors of mental health in Saudi undergraduate students. A convenience sample of 207 participants were recruited, 89% of whom were females and 94% were single. The measures included questionnaires on the level of exposure and the perceived impact of COVID-19, a physical activity measure, GAD-7, PHQ-9, and PSQI. The results indicated that approximately 43% of participants exhibited moderate anxiety, and 50% were at risk of depression. Overall, 63.93% of students exposed to strict quarantine for at least 14 days (n = 39) exhibited a high risk of developing depression (χ2(1) = 6.49, p < 0.05, ϕ = 0.18). A higher risk of depression was also found in students whose loved ones lost their jobs (χ2(1) = 4.24, p < 0.05, ϕ = 0.14). Moreover, there was also a strong association between depression and anxiety (ß = 0.33, p < 0.01), sleep quality (ß = 0.32, p < 0.01), and the perceived negative impact of COVID-19 on socio-economic status (ß = 0.26, p < 0.05), explaining 66.67% of depression variance. Our study highlights the socio-economic impact of this pandemic and the overwhelming prevalence of depression.

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The goal of this systematic review was to determine the efficacy and acceptability of telerehabilitation in physical therapy (PT) and parental acceptance during the COVID-19 pandemic in children. In 2021, an electronic search of academic articles was performed using databases such as Embase, PubMed and Scopus. One-hundred and one articles did not satisfy the eligibility criteria after deleting duplicates and reviewing abstracts, while 16 papers did not meet eligibility after reviewing complete texts. Hence, full texts for 13 articles were retrieved, which were incorporated in the review. All these studies were observational studies assessing the effectiveness and acceptability of telerehabilitation in PT required for diverse conditions in children during the COVID-19 pandemic. All included studies revealed a positive effect of telerehabilitation in PT during the COVID-19 pandemic in children with different conditions. Moreover, the included studies revealed that both rehabilitation professionals and parents or caregivers of children were satisfied with the telerehabilitation services provided remotely. Thus, telerehabilitation appears to be a suitable and convenient strategy to offer remote services to children in need but cannot visit in person due to COVID-19. The existing evidence shows that telerehabilitation can be considered effective for children who need PT for any health condition mainly during the pandemic. However, due to the dearth of studies in this area, exploring this topic is recommended mostly in low-middle-income countries with poor access to health care services and limited resources.

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Hypertension is associated with increased production and circulation of vasoconstrictors, resulting in enhanced signalling through their cognate G protein-coupled receptors (GPCR). Prolonged vasoconstrictor GPCR signalling increases arterial contraction and stimulates signalling pathways that promote vascular smooth muscle cell (VSMC) proliferation, contributing to the development of atherosclerotic plaques, re-stenosis lesions and vascular remodelling. GPCR signalling through phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) promotes VSMC proliferation. In VSMC, G protein-coupled receptor kinase 2 (GRK2) is known to regulate numerous vasoconstrictor GPCRs and their downstream signalling pathways. As GRK2 is implicated in controlling various aspects of cellular growth, we examined whether GRK2 could affect VSMC proliferation. Using two indices of cell growth, we show that PI3K inhibition and depletion of GRK2 expression produced a similar ablation of pro-proliferative vasoconstrictor-stimulated VSMC growth. Furthermore, GRK2-knockdown ablated the sustained phase of endothelin-1 and angiotensin-II-stimulated Akt phosphorylation, whilst the peak (5 min) phase was unaffected. Conversely, the GRK2 inhibitor compound 101 did not affect vasoconstrictor-driven Akt phosphorylation. Vasoconstrictor-stimulated phosphorylation of the Akt substrates GSK3α and GSK3ß was ablated following RNAi-mediated GRK2 depletion, or after PI3K inhibition. Moreover, GRK2 knockdown prevented endothelin-1 and angiotensin-II from increasing cyclin D1 expression. These data suggest GRK2 expression is essential to facilitate vasoconstrictor-driven VSMC proliferation through its ability to promote efficient prolonged PI3K-Akt signalling, and thus relieve the GSK3-mediated block on cell cycling. Considering VSMC GRK2 expression increases early in the development of hypertension, this highlights the potential for GRK2 to promote VSMC growth and exacerbate hypertensive pathophysiological vascular remodelling.

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The main objectives of this study were to evaluate the short-term effects of resisted sprint and plyometric training on sprint performance together with lower limb physiological and functional performance in collegiate football players. Ninety collegiate football players participated in this three-arm, parallel group randomized controlled trial study. Participants were randomly divided into a control group and two experimental groups: resisted sprint training (RST) (n = 30), plyometric training (PT) (n = 30), and a control group (n = 30). Participants received their respective training program for six weeks on alternate days. The primary outcome measures were a knee extensor strength test (measured by an ISOMOVE dynamometer), a sprint test and a single leg triple hop test. Measurements were taken at baseline and after 6 weeks post-training. Participants, caregivers, and those assigning the outcomes were blinded to the group assignment. A mixed design analysis of variance was used to compare between groups, within-group and the interaction between time and group. A within-group analysis revealed a significant difference (p < 0.05) when compared to the baseline with the 6 weeks post-intervention scores for all the outcomes including STN (RST: d = 1.63; PT: d = 2.38; Control: d = 2.26), ST (RST: d = 1.21; PT: d = 1.36; Control: d = 0.38), and SLTHT (RST: d = 0.76; PT: d = 0.61; Control: d = 0.18). A sub-group analysis demonstrated an increase in strength in the plyometric training group (95% CI 14.73 to 15.09, p = 0.00), an increase in the single leg triple hop test in the resisted sprint training group (95% CI 516.41 to 538.4, p = 0.05), and the sprint test was also improved in both experimental groups (95% CI 8.54 to 8.82, p = 0.00). Our findings suggest that, during a short-term training period, RST or PT training are equally capable of enhancing the neuromechanical capacities of collegiate football players. No adverse events were reported by the participants.

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All physiological events in living organisms originated as specific chemical/biochemical signals on the cell surface and transmitted into the cytoplasm. This signal is translated within milliseconds-hours to a specific and unique order required to maintain optimum performance and homeostasis of living organisms. Examples of daily biological functions include neuronal communication and neurotransmission in the process of learning and memory, secretion (hormones, sweat, and saliva), muscle contraction, cellular growth, differentiation and migration during wound healing, and immunity to fight infections. Among the different transducers for such life-dependent signals is the large family of G protein-coupled receptors (GPCRs). GPCRs constitute roughly 800 genes, corresponding to 2% of the human genome. While GPCRs control a plethora of pathophysiological disorders, only approximately one-third of GPCR families have been deorphanized and characterized. Recent drug data show that around 40% of the recommended drugs available in the market target mainly GPCRs. In this review, we presented how such system signals, either through G protein or via other players, independent of G protein, function within the biological system. We also discussed drugs in the market or clinical trials targeting mainly GPCRs in various diseases, including cancer.

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This study compares the effects of electromyographic-biofeedback (EMG-BF)-guided isometric quadriceps strengthening with patellar taping and isometric exercise alone in patellofemoral pain syndrome (PFPS) among young adult male athletes. Sixty young adult male athletes with PFPS participated in the study. Participants were randomly divided into two groups: (1) EMG-BF-guided isometric exercise training with patellar taping (experimental group, n = 30), and (2) sham EMG-BF training with an isometric exercise program (control group, n = 30). Participants conducted their respective exercise programs for five days per week across four weeks. Study outcomes were pain (measured by the visual analog scale), functional disability (measured by the Kujala Anterior Knee Pain scale), and quadriceps strength (measured by an ISOMOVE dynamometer). Measurements were taken at baseline, Week 2, Week 4, and during a follow-up at Week 6. The experimental group demonstrated significantly lower VAS score at Weeks 2 and 4 compared to that of the control group (p = 0.008 and 0.0005, respectively). The score remained significantly lower at the Week 6 follow-up compared to the control group (p = 0.0005). There were no differences in knee function at Weeks 2 and 4 between the two groups (p = 0.086 and 0.171, respectively); however, the experimental group showed significantly better knee function at Week 6 compared to the control group (p = 0.002). There were no differences in quadriceps strength at Week 2 between the two groups (p = 0.259); however, the experimental group demonstrated significantly higher quadriceps strength at Weeks 4 and 6 compared to the control group (p = 0.0008). Four weeks of EMG-BF supplementation training with patellar taping demonstrated significant improvements in pain intensity, functional disability, and quadriceps muscle strength in young adult male athletes with PFPS.

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