Fei Fang

ORCID: 0000-0002-9079-1330
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About
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Research Areas
  • RNA modifications and cancer
  • Extracellular vesicles in disease
  • Metabolism and Genetic Disorders
  • Immune cells in cancer
  • MicroRNA in disease regulation
  • Chromatin Remodeling and Cancer
  • Atherosclerosis and Cardiovascular Diseases
  • Mitochondrial Function and Pathology
  • Pelvic floor disorders treatments
  • Cell Adhesion Molecules Research
  • interferon and immune responses
  • Signaling Pathways in Disease
  • Pelvic and Acetabular Injuries
  • Phagocytosis and Immune Regulation
  • Coronary Interventions and Diagnostics
  • Hernia repair and management
  • Genetics and Neurodevelopmental Disorders
  • Cancer-related molecular mechanisms research
  • Protease and Inhibitor Mechanisms
  • Angiogenesis and VEGF in Cancer
  • Phytochemical Studies and Bioactivities
  • NF-κB Signaling Pathways
  • Mechanisms of cancer metastasis
  • Alkaline Phosphatase Research Studies
  • Hippo pathway signaling and YAP/TAZ

West China Medical Center of Sichuan University
2020-2025

Sichuan University
2022-2025

West China Hospital of Sichuan University
2025

Tibet Autonomous Region People's Hospital
2025

Third People's Hospital of Huzhou
2024

Huzhou University
2024

Beijing Children’s Hospital
2015-2023

Capital Medical University
2015-2023

Nanjing University of Chinese Medicine
2023

The University of Texas Southwestern Medical Center
2015-2022

Lipogenesis in liver is highest the postprandial state; insulin activates SREBP-1c, which transcriptionally genes involved FA synthesis, whereas glucose carbohydrate-responsive element-binding protein (ChREBP), both glycolysis and synthesis. Whether SREBP-1c ChREBP act independently of one another unknown. Here, we characterized mice with liver-specific deletion (L-Chrebp−/− mice). Hepatic deficiency resulted reduced mRNA levels glycolytic lipogenic enzymes, particularly response to sucrose...

10.1194/jlr.m081836 article EN cc-by Journal of Lipid Research 2018-01-15

Rationale: Atherosclerosis is characterized by lipid accumulation, plaque formation, and artery stenosis.The pharmacological treatment a promising therapy for atherosclerosis, but this approach faces major challenges such as targeted drug delivery, controlled release, non-specific clearance.Methods: Based on the finding that cathepsin k (CTSK) enzyme enriched in atherosclerotic lesions, we constructed an integrin αvβ3 CTSK-responsive nanoparticle to control release of rapamycin (RAP)...

10.7150/thno.70896 article EN cc-by Theranostics 2022-01-01

Chronic inflammation, inflicted by the spillover of proinflammatory mediators, links metabolic dysfunction to nonalcoholic steatohepatitis (NASH). The epigenetic maneuverings that underscore accelerated synthesis mediators in response nutritional inputs are not clearly defined. Here we report ATP-dependent chromatin remodeling proteins Brahma-related gene 1 (Brg1) and Brahma (Brm) were up-regulated vitro cultured hepatocytes treated with free fatty acid or glucose vivo animal models NASH....

10.1002/hep.26207 article EN Hepatology 2012-12-27

Rationale: Endothelial dysfunction inflicted by inflammation is found in a host of cardiovascular pathologies. One hallmark event this process the aggregation and adhesion leukocyte to vessel wall mediated upregulation molecules (CAM) endothelial cells at transcriptional level. The epigenetic modulator(s) CAM transactivation its underlying pathophysiological relevance remain poorly defined. Objective: Our goal was determine involvement Brahma related gene 1 (Brg1) (Brm) pathogenesis...

10.1161/circresaha.113.301296 article EN Circulation Research 2013-08-21

Chronic inflammation underscores the pathogenesis of a range human diseases. Lipopolysaccharide (LPS) elicits strong pro-inflammatory response in macrophages via transcription factor NF-κB. The epigenetic mechanism underlying LPS-induced is not completely appreciated. Herein we describe role for myocardin related A, or MRTF-A, this process. MRTF-A over-expression potentiated while silencing dampened NF-κB dependent transcription. deficiency also alleviated synthesis mediators mouse model...

10.1242/jcs.152314 article EN Journal of Cell Science 2014-01-01

Significance Famine kills millions of people each year. Survival requires the maintenance blood glucose. depletes body fat, thereby removing a source energy for hepatic glucose production. Here we used mouse model fat depletion to show that growth hormone (GH) maintains sugar by stimulating autophagy, process which liver digests its organelles provide and substrates producing When fat-depleted mice are fasted, their stomachs secrete ghrelin, GH secretagogue. The resultant elevation in...

10.1073/pnas.1423643112 article EN Proceedings of the National Academy of Sciences 2015-01-12

Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to host of diseases when aberrantly activated. The underlying epigenetic mechanism not completely understood. We report here MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, primary human mouse an animal model systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling...

10.1038/s41598-017-00301-w article EN cc-by Scientific Reports 2017-03-09

Epithelial–mesenchymal transition (EMT) mediated by fluid shear stress (FSS) in the tumor microenvironment plays an important role driving metastasis of malignant tumor. As a mechanotransducer, Yes‐associated protein (YAP) is known to translocate into nucleus initiate transcription genes involved cell proliferation upon extracellular biophysical stimuli. Here, we showed that FSS facilitated cytoskeleton rearrangement hepatocellular carcinoma cells, which led release YAP from its binding...

10.1002/1878-0261.13061 article EN cc-by Molecular Oncology 2021-07-14

Increased synthesis of endothelin-1 (ET-1) by human vascular endothelial cells (HVECs) in response to hypoxia underscores persistent vasoconstriction observed patients with pulmonary hypertension. The molecular mechanism whereby stimulates ET-1 gene transcription is not well understood. Here we report that megakaryocytic leukemia 1 (MKL1) potentiated hypoxia-induced transactivation HVECs. Disruption MKL1 activity either a dominant negative mutant or small interfering RNA mediated knockdown...

10.1093/nar/gkt311 article EN cc-by-nc Nucleic Acids Research 2013-04-26

Enhanced interaction between vascular endothelial cells and circulating leukocytes, as a result of transcriptional activation cell adhesion molecules (CAM), helps establish proinflammatory milieu contributing to the pathogenesis chronic hypoxia-induced pulmonary hypertension. The molecular switch that dictates CAM transactivation is not clearly defined. Our goal was determine involvement modulator megakaryocytic leukemia 1 (MKL1), also known myocardin-related transcription factor A (MRTF-A),...

10.1161/hypertensionaha.114.04585 article EN Hypertension 2015-02-03

Establishment of an inflammatory milieu following elevated leukocyte adhesion to the vascular endothelium, which is mediated by transcriptional activation cell molecules (CAMs), contributes pathogenesis chronic hypoxia-induced pulmonary hypertension (HPH). The epigenetic switch that dictates CAM transactivation in response hypoxia endothelial cells leading up HPH not fully appreciated. We report here brahma-related gene 1 (Brg1) and brahma (Brm), two catalytic components mammalian chromatin...

10.1093/cvr/cvt214 article EN Cardiovascular Research 2013-09-16

Endothelin (ET-1) was initially identified as a potent vasoconstrictor contributing to the maintenance of vascular rhythm. Later studies have implicated ET-1, when aberrantly up-regulated within vasculature, in range human pathologies associated with disruption homeostasis. ET-1 has been shown invoke strong pro-inflammatory response smooth muscle cells (VSMCs); underlying mechanism, however, remains elusive. Here, we report that transcriptional modulator MRTF-A mediates activation mediators...

10.1093/nar/gku776 article EN cc-by-nc Nucleic Acids Research 2014-08-26

Background: Cancer-associated fibroblasts (CAFs) are of considerable importance in tumor progression by interacting with the microenvironment. However, hidden mechanism explaining how cells interact CAFs mechanical microenvironment remains largely unknown. Methods: We highlighted exosomes as mediator modulating interaction between liver cancer and under conditions. The normal hepatic stellate LX2 were exposed to medium or from HepG2 without fluid shear stress subjection, activation markers...

10.31083/j.fbl2703104 article EN cc-by Frontiers in Bioscience-Landmark 2022-03-17
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