A5004356290- Cardiac Fibrosis and Remodeling
- Peptidase Inhibition and Analysis
- Atherosclerosis and Cardiovascular Diseases
- Nitric Oxide and Endothelin Effects
- Eicosanoids and Hypertension Pharmacology
- Cancer, Hypoxia, and Metabolism
- Lipid metabolism and disorders
- Metal complexes synthesis and properties
- Metal-Catalyzed Oxygenation Mechanisms
- Caveolin-1 and cellular processes
- Cardiac electrophysiology and arrhythmias
- Heat shock proteins research
- Vascular anomalies and interventions
- Lipoproteins and Cardiovascular Health
- Atrial Fibrillation Management and Outcomes
- Extracellular vesicles in disease
- Angiogenesis and VEGF in Cancer
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cell death mechanisms and regulation
- Cardiac Structural Anomalies and Repair
- Cardiac Arrhythmias and Treatments
- Pulmonary Hypertension Research and Treatments
- Cancer-related molecular mechanisms research
- Hormonal Regulation and Hypertension
- Antioxidant Activity and Oxidative Stress
Harbin Medical University
2018-2024
The First Affiliated Hospital, Sun Yat-sen University
2017-2023
Sun Yat-sen University
2017-2023
Abstract Cardiac ischemia–reperfusion (I/R) injury is a pathological process resulting in cardiomyocyte death. The present study aims to evaluate the role of long noncoding RNA Injury-Related Bclaf1-Inhibiting LncRNA (lncCIRBIL) on cardiac I/R and delineate its mechanism action. level lncCIRBIL reduced hearts. Cardiomyocyte-specific transgenic overexpression reduces infarct area following injury. Knockout mice exacerbates Qualitatively, same results are observed vitro. LncCIRBIL directly...
ASPP1 (apoptosis stimulating of p53 protein 1) is critical in regulating cell apoptosis as a cofactor to promote its transcriptional activity the nucleus. However, whether cytoplasmic affects nuclear trafficking and role cardiac diseases remains unknown. This study aims explore mechanism by which modulates subsequent contribution ischemia/reperfusion (I/R) injury.The immunofluorescent staining showed that under normal condition colocalized cytoplasm neonatal mouse ventricular cardiomyocytes,...
Nonalcoholic fatty liver disease (NAFLD) is the most common disorder with high morbidity and mortality. The current study aims to explore role of Cullin-associated neddylation-dissociated protein 1 (CAND1) in development NAFLD underlying mechanisms. CAND1 reduced male patients fat diet (HFD)-fed mice. alleviates palmitate (PA) induced lipid accumulation vitro. Hepatocyte-specific knockout exacerbates HFD-induced injury HFD-fed mice, while hepatocyte-specific knockin ameliorates these...
Endothelial-to-mesenchymal transition (EndMT), the process by which an endothelial cell (EC) undergoes a series of molecular events that result in mesenchymal phenotype, plays important role atherosclerosis. 1-Palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC), derived from oxidation 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphatidylcholine, is proinflammatory lipid found atherosclerotic lesions. Whether POVPC promotes EndMT and how simvastatin influences POVPC-mediated...
We previously demonstrated that circulating extracellular vesicles (EVs) from patients with valvular heart disease (VHD; vEVs) contain inflammatory components and inhibit endothelium-dependent vasodilation. Neutrophil chemotaxis plays a key role in renal dysfunction, dexmedetomidine (DEX) can reduce dysfunction cardiac surgery. However, the roles of vEVs neutrophil effects DEX on are unknown. Here, we investigated impact kidneys influence vEVs. Circulating EVs were isolated healthy subjects...
Abstract Introduction: Deficiency of testosterone was associated with the susceptibility atrial fibrillation (AF). Angiotensin‐II (AngII) receptor antagonists were shown to reduce AF by improving electrical remodeling. This study investigated effects and mechanism valsartan, an AngII antagonist, on deficiency. Methods Results: Five‐week‐old male ICR mice castrated valsartan administered orally (50 mg/kg/d). High‐frequency stimulation method used induce arrhythmia. Patch‐clamp technique for...
<title>Abstract</title> In the healing process of myocardial infarction, cardiac fibroblasts are activated and serious fibrosis developed, which eventually leads to remodeling heart failure. Our recent study showed that ASPP1 (apoptosis stimulating p53 protein 1) promotes cardiomyocyte apoptosis by enhancing nuclear trafficking p53. As is a key regulator fibroblast activation, we thus explored influence on molecular mechanisms related p53.Here, observed was increased after 4 weeks infarction...
The exact mechanisms of atherosclerosis remian unclear. Endothelial to mesenchymal transition (EndMT) plays an important role in atherosclerosis. 1‐Palmitoyl‐2‐(5‐oxovaleroyl)‐sn‐glycero‐3‐phosphocholine (POVPC), the oxidation product oxidized low‐density lipoprotein, is phospholipid and has been found atherosclerotic lesions. We recently demonstrated that POVPC could impair endothelial function induce cell apoptosis. However, effects on EndMT are Human aortic cells were treated with for...