A5086233625- Extracellular vesicles in disease
- Tissue Engineering and Regenerative Medicine
- Cardiac Fibrosis and Remodeling
- Pluripotent Stem Cells Research
- Phagocytosis and Immune Regulation
- RNA Interference and Gene Delivery
- Hippo pathway signaling and YAP/TAZ
- Congenital heart defects research
- Electrospun Nanofibers in Biomedical Applications
- CRISPR and Genetic Engineering
- Mechanical Circulatory Support Devices
- Cardiovascular Disease and Adiposity
- Cardiac Ischemia and Reperfusion
- RNA Research and Splicing
- Platelet Disorders and Treatments
- Cardiac Structural Anomalies and Repair
- RNA modifications and cancer
- MicroRNA in disease regulation
- Coronary Interventions and Diagnostics
- Cardiac and Coronary Surgery Techniques
- Mesenchymal stem cell research
- Cell death mechanisms and regulation
- Neuroscience and Neural Engineering
- Atherosclerosis and Cardiovascular Diseases
- Lipid metabolism and disorders
Zhongshan Hospital
2019-2024
Shanghai Clinical Research Center
2022-2024
Fudan University
2019-2024
National Health and Family Planning Commission
2024
University of North Carolina at Chapel Hill
2023-2024
University of North Carolina Health Care
2024
National Clinical Research Center for Digestive Diseases
2023
Stem cell-derived extracellular vesicles (EVs) have been demonstrated to be effective in heart repair and regeneration post infarction. However, the poor homing efficiency low yields of these therapeutics remain major obstacles before they can used clinic. To improve delivery EVs ischemia-injured myocardium, we modified mesenchymal stem cell (MSC)-derived with monocyte mimics through method membrane fusion. Monocyte mimic-bioinspired MSC-EVs (Mon-Exos) exhibited enhanced targeting injured...
Abstract Inflammatory modulations focusing on macrophage phenotype are promising candidates to promote better cardiac healing post myocardial ischemia‐reperfusion (MI/R) injury. However, the peak of monocyte/macrophage recruitment is later than time when enhanced permeability and retention effect disappears, which greatly increases difficulty reprogramming macrophages through systemic administration. Meanwhile, inability nanomaterials release their contents specific intracellular locations...
Therapeutic angiogenesis is one promising strategy for the treatment of ischemic heart disease, which leading cause death globally. In recent years, extracellular vesicles (EVs) have quickly gained much attention as a cell-free approach to stimulate angiogenesis. However, clinical applications EVs are limited by their insufficient targeting capability. Herein, we introduce method enhance therapeutic based on platelet membrane-engineered EVs.Platelet-mimetic (P-EVs) were fabricated fusing...
Abstract Efferocytosis, mediated by the macrophage receptor MerTK (myeloid‐epithelial‐reproductive tyrosine kinase), is a significant contributor to cardiac repair after myocardial ischemia‐reperfusion (MI/R) injury. However, death of resident macrophages (main effector cells), inactivation （main receptor), and overexpression “do not eat me” signals (brake signals, such as CD47), collectively lead impediment efferocytosis in post‐MI/R heart. To date, therapeutic strategies targeting...
Acute myocardial infarction (MI) induces a sterile inflammatory response that may result in poor cardiac remodeling and dysfunction. Despite the progress anti-cytokine biologics, anti-inflammation therapy of MI remains unsatisfactory, due largely to lack targeting complexity cytokine interactions. Based on nature chemotaxis cytokine-binding properties neutrophils, we fabricated biomimetic nanoparticles for targeted broad-spectrum MI. By fusing neutrophil membranes with conventional...
Resolvin D1 (RvD1) has been shown to provide effective protection against ischemia-reperfusion injury in multiple vital organs such as the heart, brain, kidney. However, clinical translational potential of systemic administration RvD1 treatment is greatly limited due biological instability and lack targeting ability. Combining natural inflammatory response reactive oxygen species (ROS) overproduction after reperfusion injury, we developed a platelet-bionic, ROS-responsive delivery platform....
Abstract CD47‐SIRPα axis is an immunotherapeutic target in tumor therapy. However, current monoclonal antibody targeting associated with on‐target off‐tumor and antigen sink effects, which significantly limit its potential clinical application. Herein, a biomimetic nano‐degrader developed to inhibit site‐specific manner through SIRPα degradation, efficacy acute myocardial infarction (AMI) evaluated. The constructed by hybridizing liposome red blood cell (RBC) membrane (RLP), mimics the CD47...
Endothelial cells are a heterogeneous population with various organ-specific and conserved functions that critical to organ development, function, regeneration. Here we report Sox17-Erg direct reprogramming approach uses cardiac fibroblasts create differentiated endothelial demonstrate endothelial-like molecular physiological in vitro vivo. Injection of these induced into myocardial infarct sites after injury results improved vascular perfusion the scar region. Furthermore, use genomic...
Adult mammalian cardiomyocytes (CMs) retain a limited proliferative ability, which is insufficient for the repair of CM loss in ischemic cardiac injury. Regulation Hippo signaling pathway to promote endogenous proliferation has emerged as promising strategy heart regeneration. Previous studies have shown that microRNA cluster miR302–367 negatively regulates pathway, promoting proliferation. In this study, we identified another microRNA, miR-10b, and promotes cell human embryonic stem...
Aortic valve disease is the most common valvular heart leading to replacement. The efficacy of pharmacological therapy for aortic limited by high mechanical stress at valves impairing binding rate. We aimed identify nanoparticle coating with entire platelet membranes fully mimic their inherent multiple adhesive mechanisms and target sclerotic apolipoprotein E-deficient (ApoE-/-) mice based on sites capacity under shear stress.Considering potent interaction membrane glycoproteins components...
Cardiovascular disease is one of the major causes death worldwide. Limited proliferative capacity adult mammalian cardiomyocytes has prompted researchers to exploit regenerative therapy after myocardial injury, such as infarction, attenuate heart dysfunction caused by injury. Direct cardiac reprogramming a recently emerged promising approach repair damaged myocardium directly converting resident fibroblasts into cardiomyocyte-like cells. The achievement in vivo direct been shown, multiple...
Abstract Poor cell homing limits the efficacy of cardiac cellular therapy. The peptide, cysteine-arginine-glutamic acid-lysine-alanine (CREKA), targets fibrin effectively which is involved in repair process tissue injury. Here, we assessed if CREKA-modified stem cells had enhanced fibrin-mediated ability resulting better functional recovery and structural preservation a rat myocardial injury model. mesenchymal (CREKA-MSCs) were obtained via membrane fusion with liposomes. targeting...
The promise of regeneration therapy for restoration damaged myocardium after cardiac ischemic injury relies on targeted delivery proliferative molecules into cardiomyocytes whose healing benefits are still limited owing to severe immune microenvironment due local high concentration proinflammatory cytokines. Optimal therapeutic strategies therefore in urgent need both modulate immunity and deliver molecules. Here, we addressed this unmet by developing neutrophil-mimic nanoparticles NM@miR,...
Direct reprogramming has revolutionized the fields of stem cell biology and regenerative medicine. Targeted transdifferentiation cells in situ holds significant promise treating a large swathe illness injury including cardiovascular disease. However, much remains unknown about molecular mechanisms direct reprogramming, particularly its post-transcriptional regulation, role m6a RNA modification. Here, by characterizing early changes methylome during fibroblasts toward three distinct...
Abstract The efferocytosis of apoptotic cardiomyocytes (CMs) after acute myocardial infarction (AMI) is required for inflammation resolution and cardiac repair. However, this process would be impaired by the interaction elevated CD47 on CMs with receptor signal-regulatory protein alpha (SIRPα) macrophages. Herein, based receptor-mediated internalization, we developed senescent RBC-mimetic liposome (RLP) as a nano-degrader to promote SIRPα degradation inhibit CD47-SIRPα axis transiently....