Ancheng Zheng

ORCID: 0000-0003-0929-3703
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About
Contact & Profiles
Research Areas
  • Cardiac Ischemia and Reperfusion
  • Cardiovascular Function and Risk Factors
  • MicroRNA in disease regulation
  • Mitochondrial Function and Pathology
  • Endoplasmic Reticulum Stress and Disease
  • Angiogenesis and VEGF in Cancer
  • Peptidase Inhibition and Analysis
  • Wnt/β-catenin signaling in development and cancer
  • Cardiac Imaging and Diagnostics
  • Signaling Pathways in Disease
  • Hippo pathway signaling and YAP/TAZ
  • Liver Disease Diagnosis and Treatment
  • Hepatitis B Virus Studies
  • Cancer-related molecular mechanisms research
  • Cell death mechanisms and regulation
  • Heart Failure Treatment and Management
  • Circular RNAs in diseases
  • Cardiac Structural Anomalies and Repair
  • Zebrafish Biomedical Research Applications

William Harvey Research Institute
2024-2025

Queen Mary University of London
2024-2025

XinHua Hospital
2022-2025

Shanghai Jiao Tong University
2023

Zhejiang University
2019-2021

State Key Laboratory of Diagnosis and Treatment of Infectious Diseases
2021

Myocardial infarction (MI) elicits cardiac fibroblast activation and extracellular matrix (ECM) deposition to maintain the structural integrity of heart. Recent studies demonstrate that Fap (fibroblast protein)-a prolyl-specific serine protease-is an important marker activated fibroblasts after MI.Left ventricle plasma samples from patients healthy donors were used analyze expression level FAP its prognostic value. Echocardiography histological analysis heart sections functions, scar...

10.1161/circresaha.122.320781 article EN Circulation Research 2023-02-09

BACKGROUND: Myocardial infarction (MI) elicits mitochondria reactive oxygen species (ROS) production and cardiomyocyte (CM) apoptosis. Nrf3 (nuclear factor erythroid 2-related 3) has an established role in regulating redox signaling tissue homeostasis. Here, we aimed to evaluate the mechanism of injury-induced pathological cardiac remodeling. METHODS: Global (Nrf3-KO) CM-specific (Nrf3 △CM ) knockout mice were subjected MI or ischemia/reperfusion injury, followed by functional...

10.1161/circulationaha.124.070286 article EN Circulation 2025-03-18

Abstract Aims Neointimal hyperplasia (NIH) characterized by vascular smooth muscle cell (VSMC) dysfunctions plays a critical role in many diseases including atherosclerosis and restenosis, which leads to serious ischemic complications has limited therapeutic approaches. Our previous studies confirm for nuclear factor erythroid 2-related 3 (Nrf3) VSMC differentiation. However, little is known about the functional implications of Nrf3 NIH. Methods Results Transcriptome dataset human...

10.1093/cvr/cvaf084 article EN Cardiovascular Research 2025-05-16

Background and Aims Characterized by hepatocyte steatosis, inflammation, fibrosis, NASH is a complicated process that contributes to end‐stage liver disease and, eventually, HCC. TNF‐α‐induced protein 8–like 1 (TIPE1), new member of the 8 family, has been explored in immunology oncology research; but little known about its role metabolic diseases. Approach Results Here, we show hepatocyte‐specific deletion TIPE1 exacerbated diet‐induced hepatic fibrosis as well systemic disorders during...

10.1002/hep.31801 article EN Hepatology 2021-03-13

Heart failure with preserved ejection fraction (HFpEF) is a multifariousness syndrome, account-ing for over half of heart (HF) patients receiving clinical treatment. The prevalence HFpEF rapidly increasing in the coming decades as global population ages. It becoming clearer that has lot different causes, which makes it challenging to find effective treatments. Currently, there are no proven treatments people deteriorating HF, or HFpEF. Although pathophysiologic foundations complex, excessive...

10.20944/preprints202409.2167.v1 preprint EN 2024-09-27

<h3>Background</h3> Myocardial infarction (MI) elicits mitochondria reactive oxygen species (ROS) production and cardiomyocyte apoptosis. Nrf3 (Nuclear factor erythroid 2-related 3) has an established role in regulating redox signaling tissue homeostasis. Herein, we aimed to uncover the exact potential mechanism of injury-induced cardiac remodeling. <h3>Methods</h3> Global (Nrf3-KO) cardiomyocyte-specific (NRF3△CM) knockout mice were subjected MI or ischemia/reperfusion (I/R) injury,...

10.1136/heartjnl-2024-bcs.232 article EN other-oa 2024-05-27
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