RESUMEN
BACKGROUND: Paroxysmal sympathetic hyperactivity (PSH) is a syndrome of excessive sympathetic activity, mainly occurring in severe traumatic brain injury. However, few studies have reported the frequency of PSH and its related risk factors in adult patients with brain injury. METHODS: We performed this systematic review and meta-analysis to estimate the combined incidence of PSH and the associated risk factors in adult patients with brain injury. This study was registered with the PROSPERO international prospective register of systematic reviews (https://www.crd.york. ac.uk/PROSPERO/Identifier: CRD 42021260493), and a systematic search was conducted of the scientific databases Embase, PubMed, Web of Science, Cochrane Library, and Google Scholar. All identified observational studies regarding the incidence and risk factors of PSH in adult patients with brain injury were included. Two authors extracted data independently; data were analyzed by STATA version 16. RESULTS: The search yielded 9 studies involving 1643 adult patients. PSH was detected in 438 patients. The combined incidence of PSH in adult patients with brain injury was 27.4% (95% confidence interval [CI], 0.190-0.358). The risk factors include patients' age (SMD = -0.592; I2 = 77.5%; 95% CI, -1.027 to -0.156; P = 0.008), traffic accident (odds ratio [OR], 1.783; I2 =18.0%; 95% CI, 1.128-2.820; P = 0.013), admission Glasgow Coma Scale score (SMD = -1.097; I2 =28.3%; 95% CI, -1.500 to -0.693; P = 0.000), hydrocephalus (OR, 3.936; I2 =67.9%; 95% CI, 1.144-13.540; P = 0.030), and diffuse axonal injury (OR, 4.747; I2 =71.1%; 95% CI, 1.221-18.463; P = 0.025) and were significantly associated with the presence of PSH after brain injury. CONCLUSIONS: PSH occurs in nearly a quarter of adult patients with brain injury. Patient's age, traffic accident, admission Glasgow Coma Scale score, hydrocephalus, and diffuse axonal injury were risk factors for PSH in adult patients with brain injury. These findings may contribute to novel strategies for early diagnosis and interventions that aid in the rehabilitation of patients with brain injury.
Asunto(s)
Enfermedades del Sistema Nervioso Autónomo , Lesiones Encefálicas , Lesión Axonal Difusa , Hidrocefalia , Adulto , Enfermedades del Sistema Nervioso Autónomo/epidemiología , Enfermedades del Sistema Nervioso Autónomo/etiología , Lesiones Encefálicas/complicaciones , Lesiones Encefálicas/diagnóstico , Escala de Coma de Glasgow , Humanos , Hidrocefalia/complicacionesRESUMEN
BACKGROUND: Diabetic nephropathy constitutes a large proportion of end-stage kidney failure in diabetic patients. However, the underlying molecular mechanisms remain unclear. METHODS: Db/db diabetic mouse models and high glucose (HG)-induced human renal mesangial cells (HRMCs) were used as research models in vivo and in vitro. The expression of cancer susceptibility candidate 2 (CASC2) was quantified by qRT-PCR. The regulatory role of CASC2 in cell apoptosis, inflammatory factor release, and fibrosis was verified by flow cytometry, qRT-PCR, and Western blot assay, respectively. The bioinformatics prediction software DIANA and starBase v2.0 were used to predict the putative binding sites. The interactions among CASC2, miR-144, and SOCS2 were explored by the luciferase assay and Western bolt assay. RESULTS: The expression of CASC2 in diabetic mouse models and HG-induced HRMCs was lower than that in the control (p < 0.05). Overexpression of CASC2 resulted in a decrease in the apoptosis rate, inflammatory factor release (TNF-α, IL-6, and IL-1ß), expression of cleaved caspase-3, and fibrotic proteins (fibronectin, Col-IV, and TGF-ß1) and an increase in Bcl-2 expression. Inhibition of CASC2 caused increased expression of miR-144. Furthermore, mechanistic investigations confirmed that activation of the miR-144/SOCS2 regulatory loop by overexpression of miR-144 reversed the in vitro effects of CASC2 on inhibiting cell apoptosis, inflammatory factor release, and fibrosis. In addition, simultaneous overexpression of miR-144 and SOCS2 further increased the inhibition of cell apoptosis, inflammatory factor release, and fibrosis by CASC2. CONCLUSION: CASC2 could alleviate the degree and process of apoptosis, inflammation, and fibrosis in diabetic nephropathic models by regulating the miR-144/SOCS2 axis.