A5007706452- Autophagy in Disease and Therapy
- Cardiovascular Function and Risk Factors
- Adipose Tissue and Metabolism
- Mitochondrial Function and Pathology
- Cardiac electrophysiology and arrhythmias
- Endoplasmic Reticulum Stress and Disease
- Metabolism, Diabetes, and Cancer
- Alcohol Consumption and Health Effects
- Cardiac Ischemia and Reperfusion
- Nitric Oxide and Endothelin Effects
- Ion channel regulation and function
- Pancreatic function and diabetes
- Birth, Development, and Health
- Neuroscience of respiration and sleep
- Trace Elements in Health
- Cardiomyopathy and Myosin Studies
- Sirtuins and Resveratrol in Medicine
- Neuroscience and Neuropharmacology Research
- Adipokines, Inflammation, and Metabolic Diseases
- Parkinson's Disease Mechanisms and Treatments
- Cardiovascular Disease and Adiposity
- Chemotherapy-induced cardiotoxicity and mitigation
- Eicosanoids and Hypertension Pharmacology
- Advanced Glycation End Products research
- Receptor Mechanisms and Signaling
Fudan University
2016-2025
Zhongshan Hospital
2016-2025
Renmin Hospital of Wuhan University
2015-2025
National Health and Family Planning Commission
2023-2025
Wuhan Textile University
2025
Wuhan University
2015-2025
Chinese Academy of Medical Sciences & Peking Union Medical College
2002-2025
Lanzhou University Second Hospital
2019-2025
Lanzhou University
2015-2025
Central South University
2021-2025
Impaired cardiac microvascular function contributes to diabetic cardiovascular complications although effective therapy remains elusive. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor recently approved for treatment of type diabetes, promotes glycosuria excretion and offers cardioprotective actions beyond its glucose-lowering effects. This study was designed evaluate the effect empagliflozin on injury in diabetes underlying mechanism involved with focus mitochondria. Our...
Mitochondrial fission and selective mitochondrial autophagy (mitophagy) form an essential axis of quality control that plays a critical role in the development cardiac ischemia-reperfusion (IR) injury. However, precise upstream molecular mechanism fission/mitophagy remains unclear. Dual-specificity protein phosphatase1 (DUSP1) regulates metabolism, but its physiological contribution reperfused heart, particularly influence on homeostasis, is unknown. Here, we demonstrated DUSP1 was...
Disturbed mitochondrial homeostasis contributes to the pathogenesis of cardiac ischemia reperfusion (IR) injury, although underlying mechanism remains elusive. Here, we demonstrated that casein kinase 2α (CK2α) was upregulated following acute IR injury. Increased CK2α shown be instrumental damage, cardiomyocyte death, infarction area expansion and dysfunction, whereas cardiac-specific knockout (CK2αCKO) mice were protected against injury damage. Functional assay indicated enhanced...
The present study was designed to examine the mechanism involved in mitochondrial aldehyde dehydrogenase (ALDH2)-induced cardioprotection against ischaemia/reperfusion (I/R) injury with a focus on autophagy. Wild-type (WT), ALDH2 overexpression, and knockout (KO) mice (n = 4–6 for each index measured) were subjected I/R, myocardial function assessed using echocardiographic, Langendroff, edge-detection systems. Western blotting used evaluate AMP-dependent protein kinase (AMPK), Akt,...
Ripk3-required necroptosis and mitochondria-mediated apoptosis are the predominant types of cell death that largely account for development cardiac ischemia reperfusion injury (IRI). Here, we explored effect Ripk3 on mitochondrial apoptosis. Compared with wild-type mice, infarcted area in Ripk3-deficient (Ripk3-/-) mice had a relatively low abundance apoptotic cells. Moreover, loss protected mitochondria against IRI inhibited caspase9 pathways. These protective effects deficiency were relied...
Background and Purpose The growing epidemic of obesity metabolic diseases necessitates the development novel strategies to prevent treat such diseases. Current research suggests that browning white adipose tissue (WAT) promotes energy expenditure counter obesity. Recent activation TRPV1 channels counters However, mechanism by which still remains unclear. Experimental Approach We evaluated effect dietary capsaicin induce a program in WAT activating diet‐induced using wild‐type −/− mouse...
Abstract Mitochondrial dysfunction has been implicated in the pathogenesis of nonalcoholic fatty liver disease ( NAFLD ) through poorly defined mechanisms. Melatonin supplementation found to protect function diabetes and obesity. Here, we intensively explored role mechanism melatonin development . We demonstrated that onset diet‐induced greatly caused NR 4A1 upregulation hepatocytes, leading activation DNA ‐ PK cs p53. On one hand, p53 aided Drp1 migration mitochondria consequently drove...
Abstract Platelet activation is a major (patho‐) physiological mechanism that underlies ischemia/reperfusion (I/R) injury. In this study, we explored the molecular signals for platelet hyperactivity and investigated beneficial effects of melatonin on reactivity in response to I/R After reperfusion, peroxisome proliferator‐activated receptor γ ( PPAR γ) was progressively downregulated patients with acute myocardial infarction undergoing coronary artery bypass grafting CABG ) surgery mice...
The NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin containing 3) inflammasome-mediated inflammatory responses are critically involved in the progression of atherosclerosis (AS), which is essential cause for cardiovascular diseases. Melatonin has anti-inflammatory properties. However, little known about potential effects melatonin pathological process AS. Herein, we demonstrate that suppressed prolonged inflammasome activation atherosclerotic lesions by reactive oxygen species...
FUN14 domain-containing protein 1 (Fundc1)-dependent mitophagy, mainly activated by ischemic/hypoxic preconditioning, benefits acute myocardial reperfusion injury and chronic metabolic syndrome via sustaining mitochondrial homeostasis. Mitochondrial fission plays a pathogenic role in ischemic kidney (AKI) through perturbation of quality activation apoptosis. The aim our study was to explore the Fundc1 mitophagy ischemia preconditioning (IPC)-mediated renoprotection. Proximal tubule-specific...