RESUMEN
Insulin resistance is the primary contributor to the disruption in glucose homeostasis in the body, playing a significant causative role in many metabolic diseases. Insulin resistance is characterized by compensatory insulin secretion and reduced insulin responsiveness in target organs. Dysregulation of the interaction between insulin-secreting cells and insulin-responsive target organs is an important factor driving the progression of insulin resistance. Circulating endocrine hormones are important mediators mediating the interaction between insulin-secreting cells and insulin-responsive target organs. In addition to the classical hormones secreted by endocrine glands and organ-specific hormones secreted by metabolism-related organs (adipose tissue, muscle, liver, etc.), extracellular vesicles have been recognized as a novel class of endocrine hormones with a complex composition. Extracellular vesicles can transport signaling molecules, such as miRNAs and LncRNAs, to vital organs related to insulin resistance, in a manner akin to conventional hormones. The significant role in regulating the development of insulin resistance underscores the increasing interest in extracellular vesicles as essential contributors to this process. In this review, we summarize the three types of hormones (classical hormones, organokines and extracellular vesicles) that play a regulatory role in insulin resistance, and focus on the novel endocrine hormones, extracellular vesicles, to elaborate the mechanism of extracellular vesicles' regulation of insulin resistance progress from two aspects: the impact on insulin-secreting cells and the influence on insulin-responsive target organs. In addition, this paper outlines the clinical applications of extracellular vesicles in insulin resistance. A comprehensive understanding of the regulatory mechanisms and diagnostic status of the inter-organ network in insulin resistance has great potential to advance targeted therapeutic interventions and diagnostic markers, thereby benefiting both the prevention and treatment of insulin resistance.
Asunto(s)
Vesículas Extracelulares , Resistencia a la Insulina , Humanos , Vesículas Extracelulares/metabolismo , Células Secretoras de Insulina/metabolismo , Células Secretoras de Insulina/fisiología , Insulina/metabolismo , Hormonas/metabolismo , Animales , Tejido Adiposo/metabolismo , MicroARNs/metabolismo , MicroARNs/genéticaRESUMEN
It is a consensus in the international manned space field that factors such as microgravity during the space flight can cause anxiety, depression and other important brain function abnormalities in astronauts. However, the neural mechanism at the molecular level is still unclear. Due to the limitations of research conditions, studies of biological changes in the primate brain have been comparatively few. We took advantage of -6° head-down bed rest (HDBR), one of the most implemented space analogues on the ground, to investigate the effects of simulated weightlessness on non-human primate brain metabolites. The Rhesus Macaque monkeys in the experiment were divided into three groups: the control group, the 42-day simulated weightlessness group with HDBR, and the recovery group, which had 28 days of free activity in the home cage after the HDBR. Liquid chromatography-mass spectrometry (LC-MS) was used to perform metabolomics analysis on specific brain areas of the monkeys under three experimental conditions. Our results show that simulated weightlessness can cause neurotransmitter imbalances, the amino acid and energy metabolism disorders, and hormone disturbances. But these metabolomics changes are reversible after recovery. Our study suggests that long-term brain damage in space flight might be reversible at the metabolic level. This lays a technical foundation for ensuring brain health and enhancing the brain function in future space studies.
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Reposo en Cama , Encéfalo , Inclinación de Cabeza , Macaca mulatta , Simulación de Ingravidez , Animales , Encéfalo/metabolismo , Masculino , Metabolómica , Ingravidez/efectos adversos , Neurotransmisores/metabolismo , Aminoácidos/metabolismo , Hormonas/metabolismoRESUMEN
The influence of gut microbiome, metabolites, omics, hormones, and stress on general and mental health is increasingly being recognized. Ancient cultures recognized the importance of diet and gut health on the overall health of an individual. Western science and modern scientific methods are beginning to unravel the foundations and mechanisms behind some of the ancient beliefs and customs. The gut microbiome, an organ itself, is now thought to influence almost all other organs, ranging from the brain to the reproductive systems. Gut microbiome, metabolites, hormones, and biological sex also influence a myriad of health conditions that range from mental health disorders, obesity, gastrointestinal disorders, and cardiovascular diseases to reproductive health. Here, we review the history and current understanding of the gut-brain axis bidirectional talk in various mental health disorders with special emphasis on anxiety and depressive disorders, whose prevalence has increased by over 50% in the past three decades with COVID-19 pandemic being the biggest risk factor in the last few years. The vagal nerve is an important contributor to this bidirectional talk, but other pathways also contribute, and most remain understudied. Probiotics containing Lactobacillus and Bifidobacterium species seem to have the most impact on improvement in mental health symptoms, but the challenge appears to be maintaining sustained levels, especially since neither Lactobacillus nor Bifidobacterium can permanently colonize the gut. Ancient endogenous retroviral DNA in the human genome is also linked to several psychiatric disorders, including depression. These discoveries reveal the complex and intricately intertwined nature of gut health with mental health disorders.
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Eje Cerebro-Intestino , Microbioma Gastrointestinal , Trastornos Mentales , Humanos , Microbioma Gastrointestinal/fisiología , Eje Cerebro-Intestino/fisiología , Trastornos Mentales/metabolismo , Trastornos Mentales/microbiología , Metabolómica , Hormonas/metabolismo , Estrés Psicológico/metabolismo , Estrés Psicológico/microbiología , Salud Mental , COVID-19/metabolismo , COVID-19/virología , Encéfalo/metabolismo , AnimalesRESUMEN
Hormonal changes in pregnant and lactating women significantly affect bone metabolism and overall stress levels, positioning them as a unique group within the orthodontic population. Fluctuations in estrogen, progesterone, prolactin, and other hormones are closely linked to bone remodeling and the periodontal tissue's response to inflammation caused by dental plaque. Hormones such as thyrotropin, leptin, and melatonin also play crucial roles in pregnancy and bone remodeling, with potential implications for orthodontic tooth movement. Additionally, adverse personal behaviors and changes in dietary habits worsen periodontal conditions and complicate periodontal maintenance during orthodontic treatment. Notably, applying orthodontic force during pregnancy and lactation may trigger stress responses in the endocrine system, altering hormone levels. However, these changes do not appear to adversely affect the mother or fetus. This review comprehensively examines the interaction between hormone levels and orthodontic tooth movement in pregnant and lactating women, offering insights to guide clinical practice.
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Lactancia , Humanos , Femenino , Lactancia/fisiología , Lactancia/metabolismo , Embarazo , Hormonas/metabolismo , Hormonas/sangre , Técnicas de Movimiento Dental/métodos , Remodelación Ósea/fisiologíaRESUMEN
Polymetabolic syndrome achieved pandemic proportions and dramatically influenced public health systems functioning worldwide. Chronic vascular complications are the major contributors to increased morbidity, disability, and mortality rates in diabetes patients. Nitric oxide (NO) is among the most important vascular bed function regulators. However, NO homeostasis is significantly deranged in pathological conditions. Additionally, different hormones directly or indirectly affect NO production and activity and subsequently act on vascular physiology. In this paper, we summarize the recent literature data related to the effects of insulin, estradiol, insulin-like growth factor-1, ghrelin, angiotensin II and irisin on the NO regulation in physiological and diabetes circumstances.
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Diabetes Mellitus , Óxido Nítrico , Humanos , Óxido Nítrico/metabolismo , Diabetes Mellitus/metabolismo , Animales , Ghrelina/metabolismo , Insulina/metabolismo , Factor I del Crecimiento Similar a la Insulina/metabolismo , Angiotensina II/metabolismo , Fibronectinas/metabolismo , Hormonas/metabolismo , Estradiol/farmacologíaRESUMEN
In lactating mothers, the high calcium (Ca2+) demand for milk production triggers significant bone loss1. Although oestrogen normally counteracts excessive bone resorption by promoting bone formation, this sex steroid drops precipitously during this postpartum period. Here we report that brain-derived cellular communication network factor 3 (CCN3) secreted from KISS1 neurons of the arcuate nucleus (ARCKISS1) fills this void and functions as a potent osteoanabolic factor to build bone in lactating females. We began by showing that our previously reported female-specific, dense bone phenotype2 originates from a humoral factor that promotes bone mass and acts on skeletal stem cells to increase their frequency and osteochondrogenic potential. This circulatory factor was then identified as CCN3, a brain-derived hormone from ARCKISS1 neurons that is able to stimulate mouse and human skeletal stem cell activity, increase bone remodelling and accelerate fracture repair in young and old mice of both sexes. The role of CCN3 in normal female physiology was revealed after detecting a burst of CCN3 expression in ARCKISS1 neurons coincident with lactation. After reducing CCN3 in ARCKISS1 neurons, lactating mothers lost bone and failed to sustain their progeny when challenged with a low-calcium diet. Our findings establish CCN3 as a potentially new therapeutic osteoanabolic hormone for both sexes and define a new maternal brain hormone for ensuring species survival in mammals.
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Densidad Ósea , Huesos , Encéfalo , Hormonas , Madres , Proteína Hiperexpresada del Nefroblastoma , Osteogénesis , Adolescente , Animales , Femenino , Humanos , Masculino , Ratones , Envejecimiento , Núcleo Arqueado del Hipotálamo/citología , Núcleo Arqueado del Hipotálamo/metabolismo , Huesos/citología , Huesos/metabolismo , Remodelación Ósea , Resorción Ósea/metabolismo , Encéfalo/citología , Encéfalo/metabolismo , Calcio/administración & dosificación , Calcio/metabolismo , Lactancia/metabolismo , Ratones Endogámicos C57BL , Neuronas/metabolismo , Células Madre/metabolismo , Células Madre/citología , Proteína Hiperexpresada del Nefroblastoma/metabolismo , Hormonas/metabolismoRESUMEN
Group 2 innate lymphoid cells (ILC2s) are a type of innate immune cells that produce a large amount of IL-5 and IL-13 and two cytokines that are crucial for various processes such as allergic airway inflammation, tissue repair and tissue homeostasis. It is known that damaged epithelial-derived alarmins, such as IL-33, IL-25 and thymic stromal lymphopoietin (TSLP), are the predominant ILC2 activators that mediate the production of type 2 cytokines. In recent years, abundant studies have found that many factors can regulate ILC2 development and function. Hormones synthesized by the body's endocrine glands or cells play an important role in immune response. Notably, ILC2s express hormone receptors and their proliferation and function can be modulated by multiple hormones during allergic airway inflammation. Here, we summarize the effects of multiple hormones on ILC2-driven allergic airway inflammation and discuss the underlying mechanisms and potential therapeutic significance.
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Citocinas , Inmunidad Innata , Linfocitos , Humanos , Inmunidad Innata/inmunología , Animales , Linfocitos/inmunología , Linfocitos/metabolismo , Citocinas/metabolismo , Citocinas/inmunología , Hormonas/metabolismo , Hormonas/inmunología , Inflamación/inmunología , Asma/inmunologíaRESUMEN
Metabolic-associated fatty liver disease (MAFLD) is a newly coined term that links the presence of liver steatosis (characterised by the accumulation of lipids in at least 5% of liver cells) with a condition of overall systemic metabolic dysfunction. MAFLD impacts 24-36% of the global population. As per the official guidelines, a diagnosis of MAFLD can be made when hepatosteatosis is accompanied by type 2 diabetes mellitus, overweight, obesity, or at least 2 other specific metabolic abnormalities (increased waist circumference, hypertension, dyslipidaemia, prediabetes, elevated C-reactive protein level, or increased homeostasis model assessment of insulin resistance: HOMA-IR). MAFLD is a heterogeneous illness associated with multiple diseases that impact various organs, particularly endocrine organs. Endocrinopathies can significantly influence the progression and severity of MAFLD. This paper provides a brief overview of the existing research on the connection between liver steatosis and the functioning of endocrine organs. The authors also propose dividing endocrine diseases into those having a possible, strong, and clear relationship with hepatosteatosis (for the purpose of preliminary recommendations regarding the need for monitoring the possible progression of MAFLD in these groups of patients).
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Enfermedad del Hígado Graso no Alcohólico , Humanos , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Enfermedad del Hígado Graso no Alcohólico/etiología , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/etiología , Femenino , Masculino , Hormonas/metabolismo , Hígado Graso/metabolismo , Hígado Graso/etiología , Obesidad/metabolismo , Obesidad/complicaciones , Resistencia a la Insulina , Enfermedades del Sistema Endocrino/metabolismo , Enfermedades del Sistema Endocrino/etiología , Enfermedades del Sistema Endocrino/complicacionesRESUMEN
BACKGROUND: Nanoplastics can be considered a novel contaminant for the environment because of their extensive applications in modern society, which represents a possible threat to humans. Nevertheless, the negative effect of polystyrene nanoplastics (PS-NPs) on male reproduction, fertility, and progeny outcomes is not well known. Thus, the aim of the present work was to calculate the median lethal dose (LD50) and investigate the consequences of exposure to PS-NPs (25 nm) on male reproductive toxicity. METHODS: This investigation first determined the LD50 of PS-NPs in male Wistar rats, and then in a formal study, 24 rats were distributed into three groups (n = 8): the control group; the low-dose group (3 mg/kg bw); and the high-dose group (10 mg/kg bw) of PS-NPs administered orally for 60 days. On the 50th day of administration, the fertility test was conducted. RESULTS: The LD50 was determined to be 2500 mg/kg. PS-NP administration induced significant alternations, mainly indicating mortality in the high-dose group, a significant elevation in body weight gain, declined sperm quality parameters, altered reproductive hormonal levels, thyroid endocrine disruption, an alternation of the normal histo-architecture and the histo-morphometric analysis of the testes, and impaired male fertility. CONCLUSION: Altogether, the current findings provide novel perspectives on PS-NP general toxicity with specific reference to male reproductive toxicity.
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Poliestirenos , Ratas Wistar , Reproducción , Testículo , Animales , Masculino , Testículo/efectos de los fármacos , Testículo/metabolismo , Poliestirenos/toxicidad , Ratas , Reproducción/efectos de los fármacos , Sistema Hipotálamo-Hipofisario/efectos de los fármacos , Sistema Hipotálamo-Hipofisario/metabolismo , Administración Oral , Fertilidad/efectos de los fármacos , Nanopartículas/toxicidad , Microplásticos/toxicidad , Dosificación Letal Mediana , Hormonas/metabolismo , Espermatozoides/efectos de los fármacosRESUMEN
Fluid and enzyme secretion from exocrine glands is initiated by Ca2+ signalling in acinar cells and is activated by external neural or hormonal signals. A wealth of information has been derived from studies in acutely isolated exocrine cells but Ca2+ signalling has until recently not been studied in undisrupted intact tissue in live mice. Our in vivo observations using animals expressing genetically encoded Ca2+ indicators in specific cell types in exocrine glands revealed both similarities to and differences from the spatiotemporal characteristics previously reported in isolated cells. These in vivo studies facilitate further understanding of how both neuronal and hormonal input shapes Ca2+ signalling events in a physiological setting and how these signals are translated into the stimulation of fluid secretion and exocytosis.
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Señalización del Calcio , Glándulas Exocrinas , Animales , Glándulas Exocrinas/metabolismo , Glándulas Exocrinas/fisiología , Neuronas/metabolismo , Neuronas/fisiología , Ratones , Hormonas/metabolismo , Hormonas/fisiología , Calcio/metabolismoRESUMEN
With the increasing prevalence of myopia among adolescents, the pathogenesis of this condition has garnered significant attention. Studies have discovered the expression of various hormone receptors in ocular tissues of both animals and humans. Additionally, changes in hormone levels accompany the development of myopia, although the exact relationships remain inconclusive. This article reviews the potential influences and mechanisms of action of endogenous hormones such as melatonin, serotonin, insulin, glucagon, sex hormones, vitamin D, and prostaglandins in ocular tissues including the retina, choroid, and sclera. It elaborates on the relationship between fluctuations in these hormone levels and the progression of myopia, aiming to provide guidance for exploring targets for myopia prevention and control.
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Melatonina , Miopía , Humanos , Miopía/metabolismo , Melatonina/metabolismo , Vitamina D/metabolismo , Serotonina/metabolismo , Insulina/metabolismo , Glucagón/metabolismo , Animales , Hormonas Esteroides Gonadales/metabolismo , Prostaglandinas/metabolismo , Hormonas/metabolismo , Retina/metabolismoRESUMEN
Understanding the intricate relationship between nutrition, hormonal balance, and gender-specific factors is crucial for developing targeted interventions to mitigate obesity-related endocrine disruptions and improve metabolic health. This narrative review examines the impact of various dietary patterns on hormonal regulation in both men and women, focusing on their effects on hormonal balance and metabolic health in the context of obesity. Calorie restriction, the Western diet, high-fat diets, low-CHO diets, plant-based diets, and the Mediterranean diet are analyzed in relation to their influence on obesity-related endocrine disruptions and metabolic health. Future research directions include investigating the specific mechanisms underlying dietary influences on hormonal regulation, addressing the gender-specific metabolic differences and body fat distribution, and exploring the dietary needs of individuals undergoing gender transition. Personalized dietary interventions tailored to individual metabolic and hormonal profiles are essential for optimizing health outcomes across the gender spectrum. By integrating gender-specific considerations into dietary recommendations, healthcare professionals can better support individuals in achieving optimal metabolic health and hormonal balance.
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Obesidad , Humanos , Masculino , Femenino , Factores Sexuales , Dieta , Hormonas/metabolismo , Dieta Mediterránea , Restricción Calórica , Dieta Occidental , Dieta Alta en Grasa , Patrones DietéticosRESUMEN
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.
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Esclerosis Amiotrófica Lateral , Biomarcadores , Insulina , Polipéptido Amiloide de los Islotes Pancreáticos , Humanos , Esclerosis Amiotrófica Lateral/metabolismo , Esclerosis Amiotrófica Lateral/sangre , Masculino , Femenino , Persona de Mediana Edad , Anciano , Polipéptido Amiloide de los Islotes Pancreáticos/metabolismo , Polipéptido Amiloide de los Islotes Pancreáticos/sangre , Estudios Transversales , Biomarcadores/sangre , Insulina/metabolismo , Insulina/sangre , Progresión de la Enfermedad , Leptina/sangre , Leptina/metabolismo , Péptido 1 Similar al Glucagón/metabolismo , Péptido 1 Similar al Glucagón/sangre , Péptido C/sangre , Péptido C/metabolismo , Ghrelina/metabolismo , Ghrelina/sangre , Glucagón/sangre , Glucagón/metabolismo , Adulto , Hormonas/metabolismo , Hormonas/sangreRESUMEN
Marine mammals possess a specific subcutaneous fat layer called blubber that not only insulates and stores energy but also secretes bioactive substances. However, our understanding of its role as a secretory organ in cetaceans is incomplete. To exhaustively explore the hormone-like substances produced in dolphin subcutaneous adipose tissue, we performed seasonal blubber biopsies from captive female common bottlenose dolphins (Tursiops truncatus; N = 8, n = 32) and analyzed gene expression via transcriptomics. Analysis of 186 hormone-like substances revealed the expression of 58 substances involved in regulating energy metabolism, tissue growth/differentiation, vascular regulation, immunity, and ion/mineral homeostasis. Adiponectin was the most abundantly expressed gene, followed by angiopoietin protein like 4 and insulin-like growth factor 2. To investigate the endocrine/secretory responses of subcutaneous adipose tissue to the surrounding temperature, we subsequently compared the mean expression levels of the genes during the colder and warmer seasons. In the colder season, molecules associated with appetite suppression, vasodilation, and tissue proliferation were relatively highly expressed. In contrast, warmer seasons enhanced the expression of substances involved in tissue remodeling, immunity, metabolism, and vasoconstriction. These findings suggest that dolphin blubber may function as an active secretory organ involved in the regulation of metabolism, appetite, and tissue reorganization in response to changes in the surrounding environment, providing a basis for elucidating the function of hormone-like substances in group-specific evolved subcutaneous adipose tissue.
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Delfín Mular , Grasa Subcutánea , Animales , Delfín Mular/metabolismo , Delfín Mular/genética , Grasa Subcutánea/metabolismo , Femenino , Transcriptoma , Perfilación de la Expresión Génica , Hormonas/metabolismo , Estaciones del Año , Metabolismo EnergéticoRESUMEN
INTRODUCTION: Intracranial aneurysms (IAs) occur in 3-5% of the general population and are characterized by localized structural deterioration of the arterial wall with loss of internal elastic lamina and disruption of the media. The risk of incidence and rupture of aneurysms depends on age, sex, ethnicity, and other different factors, indicating the influence of genetic and environmental factors. When an aneurysm ruptures, there is an estimated 20% mortality rate, along with an added 30-40% morbidity in survivors. The alterations in hormonal levels can influence IAs, while the rupture of an aneurysm can have various impacts on endocrine pathways and affect their outcome. AREA COVERED: This review explores the reciprocal relationship between endocrinological changes (estrogen, growth hormone, and thyroid hormones) and IAs, as well as the effects of aneurysm ruptures on endocrine fluctuations. EXPERT OPINION: Based on the data presented in this paper, we recommend further exploration into the influence of hormones on aneurysm formation and rupture. Additionally, we propose conducting endocrine assessments for patients who have experienced a rupture of IAs. Monitoring hormonal changes in patients with IAs could serve as a potential risk factor for rupture, leading to interventions in the approach to managing IAs.
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Aneurisma Intracraneal , Humanos , Aneurisma Roto , Factores de Riesgo , Hormonas Tiroideas/metabolismo , Estrógenos , Hormona del Crecimiento/metabolismo , Hormonas/metabolismoRESUMEN
This paper provides a summary of the role of nitric oxide (NO) and hormones in the development of chronic stress, anxiety, depression, and post-traumatic stress disorder (PTSD). These mental health conditions are prevalent globally and involve complex molecular interactions. Although there is a significant amount of research and therapeutic options available, the underlying mechanisms of these disorders are still not fully understood. The primary pathophysiologic processes involved in chronic stress, anxiety, depression, and PTSD include dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, the intracellular influence of neuronal nitric oxide synthase (nNOS) on transcription factors, an inflammatory response with the formation of nitrergic oxidative species, and reduced serotonergic transmission in the dorsal raphe nucleus. Despite the extensive literature on this topic, there is a great need for further research to clarify the complexities inherent in these pathways, with the primary aim of improving psychiatric care.