A5100412675- Aortic aneurysm repair treatments
- Cardiac Fibrosis and Remodeling
- Aortic Disease and Treatment Approaches
- Muscle Physiology and Disorders
- Cardiac Valve Diseases and Treatments
- Invertebrate Immune Response Mechanisms
- Signaling Pathways in Disease
- Ubiquitin and proteasome pathways
- Aquaculture disease management and microbiota
- Cancer-related molecular mechanisms research
- MicroRNA in disease regulation
- Peptidase Inhibition and Analysis
- Extracellular vesicles in disease
- RNA modifications and cancer
- Connective tissue disorders research
- Protease and Inhibitor Mechanisms
- Cardiovascular Function and Risk Factors
- Atherosclerosis and Cardiovascular Diseases
- Advanced biosensing and bioanalysis techniques
- Muscle metabolism and nutrition
- Autophagy in Disease and Therapy
- NF-κB Signaling Pathways
- Infectious Aortic and Vascular Conditions
- Immune cells in cancer
- Cytokine Signaling Pathways and Interactions
Beijing Anzhen Hospital
2016-2025
Capital Medical University
2016-2025
Beijing Institute of Water
2016-2025
Ministry of Education of the People's Republic of China
2015-2025
Northeast Forestry University
2025
Wuhan University
2025
Ministry of Education
2016-2024
South China Institute of Collaborative Innovation
2016-2024
Second Xiangya Hospital of Central South University
2024
Central South University
2016-2024
With trauma, sepsis, cancer, or uremia, animals patients experience accelerated degradation of muscle protein in the ATP-ubiquitin-proteasome (Ub-P’some) system. The initial step myofibrillar proteolysis is unknown because this proteolytic system does not break down actomyosin complexes myofibrils, even though it degrades monomeric actin myosin. Since cytokines insulin resistance are common catabolic states and will activate caspases, we examined whether caspase-3 would actomyosin. We found...
Conditions such as acidosis, uremia, and sepsis are characterized by insulin resistance muscle wasting, but whether the associated with these disorders contributes to atrophy is unclear. We examined this question in db/db mice increased blood glucose despite high levels of plasma insulin. Compared control littermate mice, weights different muscles cross-sectional areas were smaller. In protein degradation activities major proteolytic systems, caspase-3 proteasome, increased. signals that...
Inflammation plays an important role in cardiac injuries. Here, we examined the of miRNA regulating inflammation and injury during myocardial infarction. We showed that mir-155 expression was increased mouse heart after Upregulated primarily presented macrophages fibroblasts injured hearts, while pri-mir-155 only expressed macrophages. also exosomes derived from macrophages, it can be transferred into by macrophage-derived exosomes. A mimic or containing inhibited fibroblast proliferation...
Chronic kidney disease (CKD) and several other catabolic conditions are characterized by increased circulating inflammatory cytokines, defects in IGF-1 signaling, abnormal muscle protein metabolism, progressive atrophy. In these conditions, no reliable treatments successfully block the development of mice with CKD, we found a 2- to 3-fold increase myostatin expression muscle. Its pharmacological inhibition subcutaneous injections an anti-myostatin peptibody into CKD (IC50 ~1.2 nM) reversed...
Rapid over-activation of β-adrenergic receptor (β-AR) upon stress leads to cardiac inflammation, a prevailing factor that underlies heart injury. However, mechanisms by which acute β-AR stimulation induce inflammation still remain unknown. Here, we set out identify the crucial role inflammasome/interleukin (IL)-18 in initiating and maintaining inflammatory cascades insult.Male C57BL/6 mice were injected with single dose agonist, isoproterenol (ISO, 5 mg/kg body weight) or saline...
Necrotic death of macrophages has long been known to be present in atherosclerotic lesions but not studied. We examined the role receptor interacting protein (RIP) 3, a mediator necrotic cell death, atherosclerosis and found that RIP3(-/-);Ldlr(-/-) mice were no different from RIP3(+/+);Ldlr(-/-) early had significant reduction advanced lesions. Similar results observed Apoe(-/-) background mice. Bone marrow transplantation revealed loss RIP3 expression bone-marrow-derived cells is...
Interleukin-6 (IL-6) is an important cytokine participating in multiple biologic activities immune regulation and inflammation. IL-6 has been associated with cardiovascular remodeling. However, the mechanism of hypertensive cardiac fibrosis still unclear. Angiotensin II (Ang II) infusion mice increased expression heart. knockout (IL-6-/-) reduced Ang II-induced fibrosis: 1) Masson trichrome staining showed that significantly fibrotic areas wild-type mouse heart, which was greatly suppressed...
Chemokine-mediated monocyte infiltration into the damaged heart represents an initial step in inflammation during cardiac remodelling. Our recent study demonstrates a central role for chemokine receptor CXCR2 recruitment and hypertension; however, of CXCL1 its angiotensin II (Ang II)-induced remodelling remain unknown.Angiotensin (1000 ng kg-1 min-1) was administrated to wild-type (WT) mice treated with neutralizing antibody or inhibitor SB265610, knockout (CXCR2 KO) bone marrow (BM)...
Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate injury. Methods: We used dynamic transcriptome analysis of mouse heart exposed various periods identify S100a8/a9 as an early mediator. Using loss/gain-of-function understand the role in injury, we explored mechanisms through and functional experiment. Dynamic serum levels were measured patients with acute...
ABSTRACT. Muscle proteolysis from catabolic conditions, including chronic kidney disease, requires coordinated activation of both the apoptotic and ATP-ubiquitin-proteasome systems (Ub-P’some), upregulation components Ub-P’some system. Activation system is required because caspase-3 initially cleaves myofibrils, yielding substrates for plus a characteristic 14-kD actin fragment. The authors studied insulin deficiency, model accelerated muscle atrophy, to understand how regulation could be...
Advanced congestive heart failure is associated with activation of the renin-angiotensin system and skeletal muscle wasting. We previously showed that angiotensin II infusion in rats produces cachexia secondarily to increased proteolysis also decreases levels circulating IGF-1. Here we show markedly downregulates phospho-Akt activates caspase-3 muscle, leading actin cleavage, an important component proteolysis, apoptosis. These changes are blocked by muscle-specific expression IGF-1, likely...
Animal studies suggest that increased levels of circulating angiotensin II (AngII) could contribute to the loss lean body mass in chronic kidney disease, but mechanism by which this occurs is unclear. Here, AngII infusion IL-6 and its hepatic production wild-type mice, suggesting AngII-induced inflammation may trigger muscle loss. also stimulated suppressor cytokine signaling (SOCS3) muscle, led insulin receptor substrate 1 (IRS-1), thereby impairing insulin/IGF-1 enhancing protein...
Muscle wasting in chronic kidney disease (CKD) begins with impaired insulin/IGF-1 signaling, causing abnormal protein metabolism. In certain models of muscle atrophy, reduced satellite cell function contributes to but how CKD affects is unknown. Here, we found that isolated cells from mice had less MyoD, the master switch activation, and suppressed myotube formation compared control mice. vivo, delayed regeneration injured decreased MyoD myogenin expression, suggesting impairs proliferation...
Muscle wasting is associated with a number of pathophysiologic conditions, including metabolic acidosis, diabetes, sepsis, and high angiotensin II levels. Under these activation muscle protein degradation requires endogenous glucocorticoids. As the mechanism(s) underlying this dependence on glucocorticoids have not been identified, we analyzed effects in mouse model acute diabetes. Adrenalectomized, acutely diabetic mice given physiologic dose exhibited decreased IRS-1–associated PI3K...
Senescence is a recognized mechanism of cardiovascular diseases; however, its contribution to myocardial fibrosis and rupture after infarction the underlying mechanisms remain unclear. Here we showed that senescent cardiac fibroblasts markedly accumulated in heart infarction. The expression key senescence regulators, especially p53, was significantly up-regulated infarcted or hypoxia-treated fibroblasts. Furthermore, knockdown endogenous p53 by siRNA reduced hypoxia-induced cell senescence,...
Thoracic aortic aneurysm/dissection (TAAD) is characterized by excessive smooth muscle cell (SMC) loss, extracellular matrix (ECM) degradation and inflammation. In response to certain stimuli, endoplasmic reticulum (ER) stress activated regulates apoptosis Excessive promotes inflammation degeneration, leading TAAD. Therefore, we studied the role of ER in TAAD formation. A lysyl oxidase inhibitor, 3-aminopropionitrile fumarate (BAPN), was administrated induce formation mice, which showed...
Hypertensive ventricular remodeling is a common cause of heart failure. However, the molecular mechanisms regulating remain poorly understood.We used discovery-driven/nonbiased approach to identify increased activating transcription factor 3 (ATF3) expression in hypertensive heart. We loss/gain function approaches understand role ATF3 also examined through transcriptome, chromatin immunoprecipitation sequencing analysis, and vivo vitro experiments.ATF3 murine human hypertrophic Cardiac...
Abstract Osteopontin (OPN) exerts pro‐inflammatory effect and is associated with the development of abdominal aortic aneurysm (AAA). However, molecular mechanism underlying this association remains obscure. In present study, we compared gene expression profiles AAA tissues using microarray assay, found that OPN was highest expressed (>125‐fold). Furthermore, LC3 protein autophagy‐related genes including Atg4b, Beclin1/Atg6, Bnip3, Vps34 markedly upregulated in tissues. To investigate...
Objective— Inflammatory responses play a pivotal role in the pathogenesis of hypertensive cardiac remodeling. Macrophage recruitment and polarization contribute to development fibrosis. Although serum-glucocorticoid regulated kinase 1 (SGK1) is key mediator fibrosis, its regulating macrophage function leading fibrosis has not been investigated. We aimed determine mechanism by which SGK1 regulates inflammatory process, thus contributing Methods Results— After angiotensin II infusion mice,...
OBJECTIVE Mechanisms impairing wound healing in diabetes are poorly understood. To identify mechanisms, we induced insulin resistance by chronically feeding mice a high-fat diet (HFD). We also examined the regulation of phosphatidylinositol 3,4,5-trisphosphate (PIP3) during muscle regeneration because augmented IGF-1 signaling can improve regeneration. RESEARCH DESIGN AND METHODS Muscle was cardiotoxin injury, and evaluated satellite cell activation maturation HFD-fed mice. measured PIP3...