A5010687196- Cardiac Arrhythmias and Treatments
- Atrial Fibrillation Management and Outcomes
- Cardiac electrophysiology and arrhythmias
- Nerve injury and regeneration
- Cardiac Fibrosis and Remodeling
- Heart Rate Variability and Autonomic Control
- Apelin-related biomedical research
- Cardiovascular Function and Risk Factors
- Tissue Engineering and Regenerative Medicine
- Cardiac pacing and defibrillation studies
- Nitric Oxide and Endothelin Effects
- Signaling Pathways in Disease
- Neuropeptides and Animal Physiology
- Neuroscience of respiration and sleep
- Circular RNAs in diseases
- RNA modifications and cancer
- MicroRNA in disease regulation
- Cardiac Structural Anomalies and Repair
- Adenosine and Purinergic Signaling
- Cancer-related molecular mechanisms research
- Cardiac Ischemia and Reperfusion
- Cardiovascular Syncope and Autonomic Disorders
- Pulmonary Hypertension Research and Treatments
- Axon Guidance and Neuronal Signaling
- Protein Kinase Regulation and GTPase Signaling
Shandong Provincial QianFoShan Hospital
2014-2024
Shandong First Medical University
2019-2024
Affiliated Hospital of Shandong University of Traditional Chinese Medicine
2022-2024
Sun Yat-sen University
2023
Sun Yat-sen Memorial Hospital
2023
Shandong University
2006-2021
Asklepios Klinik St. Georg
2015
Sympathetic nerve hyperactivity is a primary reason for fatal ventricular arrhythmias (VAs) following myocardial infarction (MI). Pro-inflammatory cytokines produced in the paraventricular nucleus (PVN) post-MI are associated with sympathetic overexcitation; however, precise mechanism needs further investigation. Our aim was to explore of toll-like receptor 4 (TLR4) and its downstream molecular pathway mediating activity within PVN. A rat MI model developed via left anterior descending...
Abstract Mounting evidence supports the hypothesis that inflammation modulates sympathetic sprouting after myocardial infarction (MI). The myeloid P2X 7 signal has been shown to activate nucleotide‐binding and oligomerization domain‐like receptor family pyrin domain‐containing 3 (NLRP3) inflammasome, a master regulator of inflammation. We investigated whether participated in pathogenesis reinnervation MI, NLRP3/interleukin‐1β (IL‐1β) axis is involved process. explored relationship between...
Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in etiology of arrhythmias resulting sudden cardiac death; however, mechanisms responsible remain be elucidated. Although being a key immune mediator, role Notch yet explored. We investigated whether regulates macrophage responses inflammation and affects reinnervation rats undergoing MI. MI was induced by coronary artery ligation. A high level intracellular...
Inflammation-dominated sympathetic sprouting adjacent to the necrotic region has been implicated in etiology of severe ventricular arrhythmias (VAs) after myocardial infarction (MI). Thus, targeting inflammation process and innervation is an effective strategy prevent VAs clinically. Smart responsive injectable hydrogels have served as a good foundation biomedical engineering, especially for ischemia injury following MI. Herein, we selected boronic ester dynamic crosslinked bonding pH-...
Nerve growth factor (NGF) is involved in nerve sprouting, hyper-innervation, angiogenesis, anti-apoptosis, and preservation of cardiac function after myocardial infarction (MI). Positively modulating NGF expression may represent a novel pharmacological strategy to improve post-infarction prognosis. In this study, lentivirus encoding short interfering RNA (siRNA) was prepared, MI modeled the rat using left anterior descending coronary artery ligation. Rats were randomly grouped receive...
Sympathetic activation after myocardial infarction (MI) leads to ventricular arrhythmias (VAs), which can result in sudden cardiac death (SCD). The toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor-kappa B (NF-kB) axis within the hypothalamic paraventricular nucleus (PVN), a cardiac-neural sympathetic nerve centre, plays an important role causing VAs. An MI rat model and PVN-TLR4 knockdown were constructed. levels of protein detected by Western...
Sudden cardiac death caused by ventricular arrhythmias (VAs) is the main cause of high mortality in patients with myocardial infarction (MI). Sympathetic neural remodeling inflammation after MI closely associated occurrence VAs. METTL3, earliest identified m6A methyltransferase, critical mediating inflammatory responses. Our aim was to investigate whether methyltransferase METTL3 involved sympathetic post-MI and its specific mechanism.A rat model established via left coronary artery...
Abstract The kidney is the principal organ targeted by exposure to cadmium (Cd), a well‐known toxic metal. Even at low level, Cd damages glomerular filtration. However, little known about effects of on endothelium, which performs filtration function and directly interacts with in blood plasma. In this study, we cultured human renal endothelial cells (HRGECs) presence serum treatment short term (1 h) concentration μ m) Cd, mimics pattern endothelium vivo . We found that short‐term, low‐dose...
Pulmonary arterial hypertension (PAH) is a devastating disease that lacks sufficient treatment. Studies have shown the Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome contributes to PAH pathogenesis, but role of upstream molecular P2X7 (P2X7R) has remained unexplored. We investigated P2X7R in pathogenesis PAH. PH was induced by single subcutaneous injection monocrotaline (MCT) (60 mg/kg) on left pneumonectomised Sprague-Dawley rats, as validated significant increases...
Abstract Malignant ventricular arrhythmias ( VA s) following myocardial infarction MI ) is a lethal complication resulting from sympathetic nerve hyperactivity. Numerous evidence have shown that inflammation within the paraventricular nucleus PVN participates in Our aim was to explore role of Macrophage‐inducible C‐type lectin (Mincle) augmenting activity ,and whether NOD ‐like receptor family pyrin domain‐containing 3 NLRP 3) inflammasome/ IL ‐1β axis involved this activity. induced by...
Inflammation after myocardial infarction (MI) causes cardiac nerve sprouting and consequent ventricular arrhythmias (VAs). Macrophages, as major immune cells, are involved in the entire inflammation response process serve a link between sympathetic hyperinnervation by regulating growth factor (NGF) expression. Accumulating evidence shows that statins possess antiarrhythmogenic properties, aim of this study was to explore mechanism which atorvastatin ameliorates via macrophage...
To investigate the effects of semaphorin 3A (sema 3A) on cardiac autonomic regulation and subsequent ventricular arrhythmias (VAs) in post-infarcted hearts.In order to explore functions sema hearts, lentivirus-Sema 3A-shRNA negative control vectors were delivered peri-infarcted myocardium rats respectively. Meanwhile, recombinant (0.9% NaCl solution) injected intravenously into infarcted test therapeutic potential 3A. Results indicated that levels higher hearts compared with sham rats....
In randomized studies, the strategy of pulmonary vein antral isolation (PVI) plus linear ablation has failed to increase success rates for persistent atrial fibrillation (PeAF) when compared with PVI alone. Peri-mitral reentry related tachycardia due incomplete block is an important cause clinical failures a first procedure. Ethanol infusion (EI) into Marshall (EI-VOM) been demonstrated facilitate durable mitral isthmus lesion.This trial designed compare arrhythmia-free survival between and...
Importance Success rates of pulmonary vein isolation (PVI) are modest for persistent atrial fibrillation (AF). Additional linear ablation beyond PVI has not been proved superior to alone in randomized trials. Ethanol infusion the Marshall (EIVOM) facilitates at mitral isthmus and may lead improved effectiveness a strategy. Objective To determine whether with radiofrequency energy combined EIVOM added improves sinus rhythm maintenance compared patients AF. Design, Setting, Participants The...
Summary Background Inflammation‐dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in etiology of arrhythmias resulting sudden cardiac death; however, mechanisms responsible remain be elucidated. Although P2X 7 R is a key immune mediator, its role yet explored. Objective We investigated whether regulates NF‐κB and affects reinnervation rats undergoing MI. Methods Results An adenoviral vector with short hairpin RNA (shRNA)...
Overactivation of the sympathetic nerve may lead to severe ventricular arrhythmias (VAs) after myocardial infarction (MI). Thus, targeting activity is an effective strategy prevent VAs clinically. The superior cervical ganglion (SCG), extracardiac innervating cardiac muscles, has been found have a GABAergic signalling system, physiological significance which obscure. We aimed explore functional SCG post MI and whether signal system involved in process.
Abstract Ventricular arrhythmias (VAs) triggers by sympathetic nerve hyperactivity contribute to sudden cardiac death in myocardial infarction (MI) patients. Microglia‐mediated inflammation the paraventricular nucleus (PVN) is involved after MI. N6‐methyladenosine (m 6 A), most prevalent mRNA and epigenetic modification, critical for mediating cell inflammation. We aimed explore whether METTL3‐mediated m A modification microglia‐mediated MI PVN. model was established left coronary artery...
<i>Background:</i> Abnormal sympathetic innervation underlies both long-term hyperglycemia and myocardial infarction (MI). The incidence of ventricular arrhythmias (VAs) after MI is higher in diabetic than nondiabetic patients. However, the exact mechanism remains unclear. In this study, we aimed to explore neural remodeling rabbits its relationship with VAs. <i>Methods:</i> Rabbits were randomly assigned 4 groups: control, diabetes mellitus (DM), (DI). After...
The von Willebrand factor (vWF) is a plasma glycoprotein that plays an essential role in hemostasis by supporting platelet adhesion and thrombus formation response to vascular injury. Plasma levels of vWF are independent risk for patients with acute myocardial infarction (AMI); however, clinical data have demonstrated marked variation AMI, the reason which has not yet been identified. In present study, rat model ST-segment elevation AMI was established, cardiac peripheral blood collected...