A5001620061- Cardiac Fibrosis and Remodeling
- Cardiac Ischemia and Reperfusion
- Congenital heart defects research
- Mitochondrial Function and Pathology
- Circular RNAs in diseases
- MicroRNA in disease regulation
- Autophagy in Disease and Therapy
- Adipose Tissue and Metabolism
- Tissue Engineering and Regenerative Medicine
- Heart Rate Variability and Autonomic Control
- Cardiomyopathy and Myosin Studies
- Signaling Pathways in Disease
- Metabolism, Diabetes, and Cancer
- Pluripotent Stem Cells Research
- Cardiovascular Function and Risk Factors
- Calcium signaling and nucleotide metabolism
- Cellular transport and secretion
- Advanced Battery Technologies Research
- Extracellular vesicles in disease
- Cardiac Arrest and Resuscitation
- High Altitude and Hypoxia
- Viral Infections and Immunology Research
- Cardiovascular Health and Risk Factors
- Pulmonary Hypertension Research and Treatments
- Electrospun Nanofibers in Biomedical Applications
Shanghai Institute of Nutrition and Health
2015-2025
Chinese Academy of Sciences
2015-2019
Shanghai Institutes for Biological Sciences
2015-2019
Tân Tạo University
2015-2019
Shanghai Jiao Tong University
2014-2017
Abstract Human pluripotent stem cells (hPSCs)-derived cardiovascular progenitor (CVPCs) are a promising source for myocardial repair, while the mechanisms remain largely unknown. Extracellular vesicles (EVs) known to mediate cell–cell communication, however, efficacy and of hPSC-CVPC-secreted EVs (hCVPC-EVs) in infarct healing when given at acute phase infarction (MI) Here, we report cardioprotective effects secreted from hESC-CVPCs under normoxic (EV-N) hypoxic (EV-H) conditions infarcted...
Impaired autophagic flux contributes to ischemia/reperfusion (I/R)-induced cardiomyocyte death, but the underlying molecular mechanisms remain largely unexplored.To determine role of LAPTM4B (lysosomal-associated transmembrane protein 4B) in regulation and myocardial I/R injury.LAPTM4B was expressed murine hearts downregulated with (30 minutes/2 hours) injury neonatal rat cardiomyocytes hypoxia/reoxygenation (6 hours/2 injury. During reperfusion, LAPTM4B-knockout (LAPTM4B-/-) mice had a...
Abstract Pretreatment of berbamine protects the heart from ischemia/reperfusion (I/R) injury. However it is unknown whether has cardioprotection when given at onset reperfusion (postconditioning (PoC)), a protocol with more clinical impact. Autophagy upregulated in I/R myocardium and exacerbates cardiomyocyte death during reperfusion. However, autophagy regulated by berbamine. Here we investigated PoC (BMPoC) through regulation analyzing effects BMPoC on infarct size and/or cell death,...
Uncoupling protein 3 (UCP3), located in the mitochondrial inner membrane, is cardioprotective, but its mechanisms of preserving function during ischaemia/reperfusion (I/R) are not fully understood. This study investigated whether UCP3 mediates/mimics cardioprotection H2O2 preconditioning (H2O2PC) against I/R injury and downstream pathway that mediates H2O2PC- UCP3-afforded cardioprotection. H2O2PC at 20 µM for 5 min significantly improved post-ischaemic functional recovery reduced lactate...
Abstract Myocardial infarction (MI) causes excessive damage to the myocardium, including epicardium. However, whether pluripotent stem cell‐derived epicardial cells (EPs) can be a therapeutic approach for infarcted hearts remains unclear. Here, authors report that intramyocardial injection of human embryonic EPs (hEPs) at acute phase MI ameliorates functional worsening and scar formation in mouse hearts, concomitantly with enhanced cardiomyocyte survival, angiogenesis, lymphangiogenesis....
Abstract Aims Circular RNAs (circRNAs) are important players involved in a variety of physiological and pathological processes. However, their functions mechanisms during myocardial ischaemic injury protection remain largely unknown. We recently found significant alterations many circRNAs including circCHSY1 following ischaemia/reperfusion (I/R) injury, whereas exact unclear. Here, we investigated the roles acute I/R potential involved. Methods results The expression was detected...
Myocardial infarction resulting from coronary atherosclerosis is the leading cause of death in modern society. Reperfusion an essential treatment to salvage ischemia myocardium necrosis, while it also leads additional damage. Therefore, exploring effective medicines protect heart post-ischemic injury one major objectives cardiovascular research. Berbamine, a nature compound bisbenzylisochinoline alkaloids Barberry, protects ischemia/reperfusion (I/R) when given before I/R, but unknown...
Myocardial injury following ischemia/reperfusion (I/R) is a common clinical scenario in patients suffering from ischemic heart disease. An excessive production of reactive oxygen species (ROS) during the early phase reperfusion myocardial ischemia has been proposed to contribute injury. Paradoxically, ROS also recognized as trigger pro-survival signaling pathways mediating cardioprotection at low level. However, precise mechanisms for dual role have not yet fully clarified. To address this...
Background: Acute myocardial infarction (AMI) causes excessive myocardium damage, including epicardium. Cell therapy by implantation of human pluripotent stem cell (hPSC)-derived cardiovascular cells has been tested in the infarcted hearts preclinical models and clinical studies. However, whether hPSC-derived epicardial (hEPs) can be a therapeutic approach for remains unclear. AMI induces inflammatory cascades, leading to multifaceted processes injury healing, whereas it is unknown hEPs...
Reactive oxygen species (ROS) generated during early reperfusion activated signal transducer and activator of transcription 3 (STAT3) contribute to intermittent hypobaric hypoxia (IHH)-afforded cardioprotection against ischemia/reperfusion (I/R)-induced mitochondrial calcium overload, but its mechanisms are not fully understood. This study investigated whether ROS signaling STAT3 is involved in moderate hydrogen peroxide postconditioning (H 2 O PoC) mimicked IHH cardiac I/R injury the...