A5054654657- Cardiovascular Function and Risk Factors
- Cardiac Fibrosis and Remodeling
- Endoplasmic Reticulum Stress and Disease
- Mitochondrial Function and Pathology
- Signaling Pathways in Disease
- Cardiac Ischemia and Reperfusion
- Cardiovascular Effects of Exercise
- Diet and metabolism studies
- Cardiovascular Disease and Adiposity
- Apelin-related biomedical research
- Mesenchymal stem cell research
- Nitric Oxide and Endothelin Effects
- Tissue Engineering and Regenerative Medicine
- Genetics, Aging, and Longevity in Model Organisms
- Cholinesterase and Neurodegenerative Diseases
- Cerebrovascular and Carotid Artery Diseases
- Chemotherapy-induced cardiotoxicity and mitigation
- Metabolism, Diabetes, and Cancer
- Circadian rhythm and melatonin
- Pancreatic function and diabetes
- Phagocytosis and Immune Regulation
- FOXO transcription factor regulation
- Healthcare and Venom Research
- Electron Spin Resonance Studies
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
Air Force Medical University
1990-2025
Xijing Hospital
2018-2025
Oregon Health & Science University
2016
Exercise benefits to cardiac rehabilitation (CR) following stable myocardial infarction (MI). The suitable exercise duration for aged patients with coronary heart disease (CHD) remains controversial, and the underlying molecular mechanism is still unclear.18-Month-old mice after MI were randomly submitted different durations of exercise, including 15 60 min swimming training (ST) once per day, five times a week 8 weeks. Compared sedentary mice, ST, rather than significantly augmented left...
Abstract Cardiokines play an essential role in maintaining normal cardiac functions and responding to acute myocardial injury. Studies have demonstrated the heart itself is a significant source of C1q/TNF-related protein 9 (CTRP9). However, biological cardiac-derived CTRP9 remains unclear. We hypothesize responds ischemia/reperfusion (MI/R) injury as cardiokine. explored MI/R via genetic manipulation CTRP9-knockout (CTRP9-KO) animal model. Inhibition exacerbated, whereas its overexpression...
Abstract C1q-tumor necrosis factor-related protein-3 (CTRP3) is an adipokine, which exerts protective function in ischemic or diabetic heart injury. However, the role of CTRP3 cardiac hypertrophy remains unclear. The aim this study was to investigate pharmacological effects on pathological induced by hypertension. Male C57BL/6 J wild-type (WT) mice, Ctrp3 knockout and mice infected with lentivirus overexpressing mouse underwent sham surgery transverse aortic constriction (TAC) surgery. After...
Abstract Pathological cardiac hypertrophy is an independent risk factor for heart failure. Disruption of mitochondrial protein homeostasis plays a key role in pathological hypertrophy; however, the mechanism maintaining remains unclear. In this study, we investigated regulatory mechanisms hypertrophy. Wildtype (WT) mice, knockout and mice transfected with lentivirus overexpressing mouse C1q-tumor necrosis factor-related protein-3 (CTRP3) underwent transverse aortic constriction or sham...
In developed nations, myocardial infarction (MI) is one of the main causes morbidity and mortality, resulting in a significant economic burden becoming global public health problem. C1q/tumor necrosis factor-related protein 9 (CTRP9) secreted comprising variable domain, collagenous region, C-terminal trimerizing globular C1q (gC1q) domain. vivo, full-length CTRP9 (fCTRP9) can be cleaved into domain (gCTRP9). Here, we tested cardio-protective impacts fCTRP9, gCTRP9, N-terminal including...
The cover image is based on the article SLC30A4‐AS1 Mediates Senescence of Periodontal Ligament Stem Cells in Inflammatory Environments via Alternative Splicing TP53BP1 by Mei Xu et al., https://doi.org/10.1111/cpr.13778 .
Mitochondrial unfolding protein response (UPRmt) effectively resists the pathological cardiac hypertrophy and improves mitochondrial function. However, specific activation mechanism drugs that can activate UPRmt in muscle are yet to be elucidated. The aim of this study was determine regulation role on preventing by tetrahydrocurcumin (THC) explore its underlying molecular mechanism. Male C57BL/6J wild-type (WT) mice were divided into a control group subjected sham treatment for 4 weeks, test...
As heart failure develops, the utilizes ketone bodies at increased rates, indicating an adaptive stress response. Thus, increasing body availability exerts protective effects against failure. However, although it is widely used approach for availability, ketogenic diet shows limited cardioprotective This study was aimed examining of on and underlying mechanisms. Pressure overload-induced established by transverse aortic constriction (TAC) in mice. Continuous feeding 8 weeks failed to protect...
Abstract Mesenchymal stromal cells (MSCs) transplantation offers an attractive alternative in myocardial infarctive therapy. However, poor cell engraftment and survival limit their restorative capacity. C1q/tumor necrosis factor-related protein-3 (CTRP3) inhibits reverse remodeling after infarction (MI) was found to be secreted by MSCs our preliminary experiments. We examined whether the overexpression of CTRP3 improved transplanted augmented efficacy on MI silencing attenuated these...
Long-term exercise-induced metabolic adaptations occupy a central position in exercise-afforded cardiac benefits. Emerging evidence suggests that branched-chain amino acid (BCAA) catabolic defect contributes to dysfunction multiple cardiometabolic diseases. However, the role of BCAA catabolism benefits remains unknown. Here, we show exercise improves and thus reduce vulnerability myocardial ischemic injury. Exercise increased circulating levels both humans (male adolescent athletes) mice...
Myocardial ischemia-reperfusion (MI/R) is a major risk factor for cardiovascular disease. At present, reducing oxidative stress and apoptosis crucial therapeutic strategy ameliorating MI/R injury. However, there lack of drugs targeting the clinical therapy MI/R. Bergenin reportedly effective agent with antioxidative antiapoptotic activity against acute Nevertheless, roles potential mechanisms bergenin injury remain unknown. Here, we hypothesized that attenuated MI/R-induced reactive oxygen...
Gastrodia elata exhibits extensive pharmacological activity; its extract gastrodin (GAS) has been used clinically to treat cardiovascular diseases. In the present study, we examined effect of GAS in a mice model pathological cardiac hypertrophy, which was induced using transverse aortic constriction (TAC). Male C57BL/6 J underwent either TAC or sham surgery. administered post-surgically for 6 weeks and significantly improved deterioration contractile function caused by pressure overload,...
Premenopausal women have a reduced risk for cardiovascular disease. Estrogen deficiency augments cardiac inflammation and oxidative stress and, thereby, aggravates myocardial fibrosis (MF) diastolic dysfunction in hypertensive female rats. However, estrogen replacement therapy has no effect on infarction postmenopausal women. Further clinical studies showed that high blood glucose levels patients with diabetes is an important cause of MF, but the underlying mechanism unclear. To...
Abstract Injury/dysfunction of the endothelium pulmonary arteries contributes to hypoxia-induced hypertension (HPH). We investigated whether C1q/tumor necrosis factor-related protein-9 (CTRP9), a newly identified cardiovascular agent, has protective roles in development HPH. HPH was induced adult male rats by chronic hypobaric hypoxia. CTRP9 overexpression adeno-associated virus (AAV)-CTRP9 transfection attenuated increases right ventricular systolic pressure, hypertrophy index, and arterial...
Abstract Pathological cardiac hypertrophy exhibits complex and abnormal gene expression patterns progresses to heart failure. Forkhead box protein O6 (FoxO6) is a key transcription factor involved in many biological processes. This study aimed explore the role of FoxO6 hypertrophy. Three groups mice were established: wild‐type, knockout, FoxO6‐overexpressing. The received daily administration angiotensin‐II (Ang‐II) or saline for 4 weeks, after which they examined hypertrophy, fibrosis,...
Regular exercise is recommended as an important component of therapy for cardiovascular diseases in clinical practice. However, there are still major challenges prescribing optimized regimen to individual patients with established cardiac disease. Here, we tested the effects different doses on function mice myocardial infarction (MI). Exercise was introduced MI after 4 weeks surgery. Low-dose (15 min/day 8 weeks) improved mortality and by increasing 44.39% ejection fractions while inhibiting...
Abstract Heart failure is a leading cause of mortality worldwide, necessitating the development novel therapeutic and lifestyle interventions. Recent studies highlight potential role time‐restricted feeding (TRF) in prevention treatment cardiac diseases. Here, it found that TRF protected against heart at different stages mice. Metabolomic profiling revealed upregulated most circulating amino acids, acid supplementation failure. In contrast, showed mild effect on profile, but increased...
Introduction: Regular physical exercise is widely recognized for its beneficial effects on overall health. Despite emerging evidence that early-life experiences profoundly impact adult and aged health, the long-term of remain uncertain. Hypothesis: We hypothesized extends healthspan attenuates cardiovascular aging in mice. Methods: Male female C57BL/6J mice were subjected to a 3-month swimming regimen starting from 1 month age (1.5 hour per day, 5 days week), while no intervention was...
ABSTRACT Periodontal ligament stem cells (PDLSCs) are key that suppress periodontal damage during both the progression and recovery stages of periodontitis. Although substantial evidence has demonstrated incubation under an inflammatory condition may accelerate senescence PDLSCs, whether cellular in response to contributes cell dysfunction remain unexplored. In this study, we first observed inflammation‐caused PDLSC periodontitis based on comparisons matched patients, was healthy were...
The fragility of erythrocytes (RBC) from patients with acute ischemic stroke and normal age-matched control individuals was compared in the presence ionomycin various calcium ion concentrations ranging 0 to 2.5 mM after filtration through 5 µm pore diameter polycarbonate membranes at 20 cm Hg pressure. At 0.5, 1.0 1.5 mM, RBC hemolyzed a greater extent than those obtained controls. This difference is indicative abnormal homeostasis patients. Flunarizine, channel blocker, significantly...