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NEDD4-Mediated GSNOR Degradation Aggravates Cardiac Hypertrophy and Dysfunction.
Circ Res
January 2025
Key Laboratory of Drug Targets and Translational Medicine for Cardio-cerebrovascular Diseases, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Jiangsu, China (X.T., X.L., X.S., Y. Zhang, Y. Zu, Q.F., L.H., S.S., F.C., L.X., Y.J.).
Background: The decrease in S-nitrosoglutathione reductase (GSNOR) leads to an elevation of S-nitrosylation, thereby exacerbating the progression of cardiomyopathy in response to hemodynamic stress. However, the mechanisms under GSNOR decrease remain unclear. Here, we identify NEDD4 (neuronal precursor cell expressed developmentally downregulated 4) as a novel molecule that plays a crucial role in the pathogenesis of pressure overload-induced cardiac hypertrophy, by modulating GSNOR levels, thereby demonstrating significant therapeutic potential.
View Article and Find Full Text PDFVascular HIF2 Signaling Prevents Cardiomegaly, Alveolar Congestion, and Capillary Remodeling During Chronic Hypoxia.
Arterioscler Thromb Vasc Biol
January 2025
Metabolic and Immune Diseases Department, Biomedical Research Institute Sols-Morreale (IIBM), National Research Council (CSIC), Autonoma University of Madrid, Spain (T.A.-G., S.M.-T., R.C.-M., S.U.-B., S.M.-P.).
Background: Hypoxia is associated with the onset of cardiovascular diseases including cardiac hypertrophy and pulmonary hypertension. HIF2 (hypoxia-inducible factor 2) signaling in the endothelium mediates pulmonary arterial remodeling and subsequent elevation of the right ventricular systolic pressure during chronic hypoxia. Thus, novel therapeutic opportunities for pulmonary hypertension based on specific HIF2 inhibitors have been proposed.
View Article and Find Full Text PDFGinkgolide B as a biopsychosocial treatment salvages repeated restraint stress-induced amygdalar anomalies in mice.
IBRO Neurosci Rep
June 2025
Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Oyo State, Nigeria.
From preclinical and clinical findings, it has been shown that the amygdala is a critical mediator of stress and primary target for stress effects in the brain. We investigated the neuroprotective effect of Ginkgolide B (GB) in repeated restraint stress-induced behavioral deficit and amygdalar inflammation in mice. Mice were orally pre-treated with GB 20 mg/kg 1 h prior to 4 h restraint stress for 21 consecutive days.
View Article and Find Full Text PDFTargeting IGF1 to alleviate obesity through regulating energy expenditure and fat deposition.
Sci China Life Sci
January 2025
State Key Laboratory of Pharmaceutical Biotechnology, Department of Endocrinology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Model Animal Research Center, Nanjing University, Nanjing, 210061, China.
Insulin-like growth factor 1 (IGF1) is a regulator of both cellular hypertrophy and lipogenesis, which are two key processes for pathogenesis of obesity. However, the in vivo role of IGF1 in the development of obesity remains unclear. Here, we show that IGF1 expression is increased in adipose tissue in obese human patients and animal models.
View Article and Find Full Text PDFNewly synthesized proteins destined for the secretory pathway are folded and assembled in the endoplasmic reticulum (ER) and then transported to the Golgi apparatus via COPII vesicles, which are normally 60-90 nm. COPII vesicles must accordingly be enlarged to accommodate proteins larger than 90 nm, such as long-chain collagen. Key molecules involved in this enlargement are Tango1 and Tango1-like (Tali), which are transmembrane proteins in the ER encoded by the MIA3 and MIA2 genes, respectively.
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