Yi Fu

ORCID: 0000-0002-8832-9331
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About
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Research Areas
  • Aortic aneurysm repair treatments
  • Ion Channels and Receptors
  • Connective tissue disorders research
  • Electrolyte and hormonal disorders
  • Aortic Disease and Treatment Approaches
  • Ion channel regulation and function
  • Ion Transport and Channel Regulation
  • RNA modifications and cancer
  • Atherosclerosis and Cardiovascular Diseases
  • Cell Adhesion Molecules Research
  • Folate and B Vitamins Research
  • Protease and Inhibitor Mechanisms
  • Ovarian cancer diagnosis and treatment
  • Helicobacter pylori-related gastroenterology studies
  • Galectins and Cancer Biology
  • Monoclonal and Polyclonal Antibodies Research
  • Macrophage Migration Inhibitory Factor
  • Respiratory and Cough-Related Research
  • MicroRNA in disease regulation
  • Hormonal Regulation and Hypertension
  • Cancer-related gene regulation
  • Peptidase Inhibition and Analysis
  • Blood Coagulation and Thrombosis Mechanisms
  • Angiogenesis and VEGF in Cancer
  • Circular RNAs in diseases

Peking University
2015-2025

First Affiliated Hospital of Anhui Medical University
2025

Anhui Medical University
2025

Kunming Municipal Hospital of Traditional Chinese Medicine
2025

Tongji University
2024

Tongji Hospital
2024

Fudan University Shanghai Cancer Center
2024

West China Hospital of Sichuan University
2023

Mianyang Third People's Hospital
2023

Sichuan University
2023

Dietary potassium deficiency, common in modern diets, raises blood pressure and enhances salt sensitivity. Potassium homeostasis requires a molecular switch the distal convoluted tubule (DCT), which fails familial hyperkalemic hypertension (pseudohypoaldosteronism type 2), activating thiazide-sensitive NaCl cotransporter, NCC. Here, we show that dietary deficiency activates NCC, even setting of high intake, thereby causing sodium retention rise pressure. The effect is dependent on plasma...

10.1016/j.cmet.2014.12.006 article EN publisher-specific-oa Cell Metabolism 2015-01-01

Hyperhomocysteinemia (HHcy) is a risk factor for various cardiovascular diseases. However, the mechanism underlying HHcy-aggravated vascular injury remains unclear. Here we show that aggravation of abdominal aortic aneurysm by HHcy abolished in mice with genetic deletion angiotensin II type 1 (AT1) receptor and treated an AT1 blocker. We find homocysteine directly activates signalling. Homocysteine displaces limits its binding to receptor. Bioluminescence resonance energy transfer analysis...

10.1038/s41467-017-02401-7 article EN cc-by Nature Communications 2017-12-27

Whether changes in endothelial tight junctions (TJs) lead to the formation of thoracic aortic aneurysm and dissection (TAAD) serve as an early indicator therapeutic target remains elusive.Single-cell RNA sequencing analysis showed aberrant TJ expressions aortas patients with TAAD. In a β-aminopropionitrile (BAPN)-induced TAAD mouse model, function was disrupted at stage (5 10 days) observed by vascular permeability assay, while intercellular distribution crucial components significantly...

10.1093/eurheartj/ehac823 article EN European Heart Journal 2023-01-14

The pathogenesis of thoracic aortic aneurysm (TAA) in Marfan syndrome (MFS) is generally attributed to vascular smooth muscle cell (VSMC) pathologies. However, the role immune cell-mediated inflammation remains elusive. Single-cell RNA sequencing identified a subset CX3CR1+ macrophages mainly located intima roots and ascending aortas Fbn1C1041G/+ mice, further validated MFS patients. Specific elimination cells by diphtheria toxin Cx3cr1-CreERT2iDTRF/+Fbn1C1041G/+ mice efficiently ameliorated...

10.1172/jci178198 article EN cc-by Journal of Clinical Investigation 2025-01-15

Rationale: Angiotensin-converting enzyme (ACE)2 opposes the actions of angiotensin (Ang) II by degrading it to Ang 1-7. Objective: Given important role II/Ang 1-7 in atherogenesis, we investigated impact ACE2 deficiency on development atherosclerosis. Methods and Results: C57Bl6 , Ace2 knockout (KO), apolipoprotein E ( ApoE ) KO ApoE/Ace2 double mice were followed until 30 weeks age. Plaque accumulation was increased when compared mice. This associated with expression adhesion molecules...

10.1161/circresaha.110.219279 article EN Circulation Research 2010-07-30

Background— ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide coronary artery disease. However, mechanisms that link ADAMTS-7 disease risk remain elusive. We have previously demonstrated promotes vascular smooth muscle cell migration postinjury neointima formation via degradation matrix protein cartilage oligomeric protein. Because delayed endothelium repair renders...

10.1161/circulationaha.114.014072 article EN Circulation 2015-02-26

Metastasis is the main cause of cancer mortality. During this process, cells dislodge from a primary tumor, enter circulation and form secondary tumors in distal organs. It poorly understood how these manage to cross tight syncytium endothelial that lines capillaries. Such capillary transmigration would require drastic change cell shape. We have therefore developed microfluidic platform study cells. The device consists an array microchannels mimicking confined spaces encountered. A thin...

10.1039/c2lc40477j article EN Lab on a Chip 2012-01-01

Although not fully understood, the phenotypic transition of vascular smooth muscle cells exhibits at early onset pathology aortic aneurysms. Exploring key regulators that are responsible for maintaining contractile phenotype (VSMCs) may confer homeostasis and prevent aneurysmal disease. XBP1 (X-box binding protein 1), which exists in a transcriptionally inactive unspliced form (XBP1u) spliced active (XBP1s), is component response to endoplasmic reticular stress. Compared with XBP1s, little...

10.1161/circresaha.117.311450 article EN Circulation Research 2017-10-31

Background: How the extracellular matrix (ECM) microenvironment modulates contractile phenotype of vascular smooth muscle cells (VSMCs) and confers homeostasis remains elusive. Methods: To explore key ECM proteins in maintenance VSMCs, we applied protein-protein interaction network analysis to novel associated with VSMC phenotype. By combining vitro vivo genetic mice injury models, identified nidogen-2, a basement membrane glycoprotein, as protein for cell identity. Results: We collected...

10.1161/circulationaha.120.053361 article EN Circulation 2021-07-28

Phenotypic transition of vascular smooth muscle cells (VSMCs) accounts for the pathogenesis a variety diseases during early stage. Recent studies indicate metabolic reprogramming may be involved in VSMC phenotypic transition. However, definite molecules that link energy metabolism to distinct phenotype remain elusive.A carotid artery injury model was used study postinjury neointima formation as well vivo. RNA-seq analysis, cell migration assay, collagen gel contraction wire myography...

10.1161/circresaha.122.321005 article EN Circulation Research 2022-10-06

Background: The metalloprotease ADAMTS-7 (a disintegrin and metalloproteinase with thrombospondin type 1 motif 7) is a novel locus associated human coronary atherosclerosis. deletion protects against atherosclerosis vascular restenosis in rodents. Methods: We designed 3 potential vaccines consisting of distinct B cell epitopic peptides derived from conjugated the carrier protein KLH (keyhole limpet hemocyanin) as well aluminum hydroxide an adjuvant. Arterial ligation or wire injury was used...

10.1161/circulationaha.122.061516 article EN Circulation 2022-12-23

Abdominal aortic aneurysm (AAA) is a lethal cardiovascular disease, and there no proven drug treatment for this condition. In study, by using the Connectivity Map (CMap) approach, we explored naringenin, naturally occurring citrus flavonoid, as putative agent inhibiting AAA. We then validated prediction with two independent mouse models of AAA, calcium phosphate (CaPO4)-induced C57BL/6J mice angiotensin II-infused ApoE-/- mice. Naringenin effectively blocked formation AAAs progression...

10.1038/s41421-021-00363-1 article EN cc-by Cell Discovery 2022-03-01

The ECM (extracellular matrix) is a major component of the vascular microenvironment that modulates homeostasis. proteins include collagens, elastin, noncollagen glycoproteins, and proteoglycans/glycosaminoglycans. form complex matrix structures, such as basal lamina collagen elastin fibers, through direct interactions or lysyl oxidase-mediated cross-linking. Moreover, directly interact with cell surface receptors extracellular secreted molecules, exerting matricellular matricrine...

10.1161/circresaha.123.324055 article EN Circulation Research 2024-03-28

Disorders of water balance are among the most common and morbid electrolyte disturbances, reflected clinically as abnormalities in serum sodium concentration. The transient receptor potential vanilloid 4 (TRPV4) channel is postulated to comprise an element central tonicity-sensing mechanism mammalian hypothalamus, activated by hypotonic stress vitro. A nonsynonymous polymorphism TRPV4 gene gives rise a Pro-to-Ser substitution at residue 19. We show that this significantly associated with...

10.1073/pnas.0904084106 article EN Proceedings of the National Academy of Sciences 2009-08-05

Transdifferentiation of adventitial fibroblasts (AFs) into myofibroblasts plays a critical role during the vascular remodeling that occurs atherosclerosis, restenosis, and aortic aneurysm. The ubiquitination/deubiquitination regulatory system is essential for quality control proteins. involvement AF transdifferentiation remains largely unknown. In this study, we determined cylindromatosis (CYLD), deubiquitinase, in process differentiation activation vitro vivo.Transforming growth factor-β1...

10.1161/atvbaha.117.309859 article EN Arteriosclerosis Thrombosis and Vascular Biology 2017-07-28

Background: Obesity plays crucial roles in the development of cardiovascular diseases. However, mechanisms that link obesity and diseases remain elusive. Compelling evidence indicates adipokines play an important role obesity-related Here, we found a new adipokine-named family with sequence similarity 19, member A5 (FAM19A5), protein unknown function was predicted to be distantly related CC-chemokine family. We aimed test whether adipose-derived FAM19A5 regulates vascular pathology on...

10.1161/circulationaha.117.032398 article EN Circulation 2018-02-16

Vascular calcification is a prevalent complication in chronic kidney disease and contributes to increased cardiovascular morbidity mortality. XBP1 (X-box binding protein 1), existing as the XBP1u (unspliced XBP1) XBP1s (spliced forms, key component of endoplasmic reticulum stress involved vascular diseases. However, whether participates development remains unclear.We aim investigate role calcification. levels were reduced high phosphate-induced calcified smooth muscle cells, aortas from mice...

10.1161/circresaha.121.319745 article EN Circulation Research 2021-12-06

Background: Vascular endothelial cells are critical for maintaining blood pressure (BP) by releasing biologically active molecules, such as nitric oxide. A non-endothelial cell resident matricellular protein, COMP (cartilage oligomeric matrix protein), plays a pivotal role in cardiovascular homeostasis, but little is known about its regulatory effect on BP. Methods: Mice were infused with AngII (angiotensin II; 450 ng/kg per minute) 3 days via an osmotic minipump, and BP was monitored...

10.1161/hypertensionaha.121.17972 article EN Hypertension 2022-01-05

The cochlea and kidney are susceptible to aminoglycoside-induced toxicity. non-selective cation channel TRPV4 is expressed in distal tubule cells, hair cells the stria vascularis inner ear. To determine whether involved aminoglycoside trafficking, we generated a murine proximal-tubule cell line (KPT2) distal-tubule (KDT3). expression was confirmed KDT3 but not KPT2 cells. Removal of extracellular Ca(2+) significantly enhanced gentamicin-Texas-Red (GTTR) uptake by KDT3, indicative permeation...

10.1242/jcs.023705 article EN other-oa Journal of Cell Science 2008-08-06

TRPV4, a renally expressed nonselective cation channel of the transient receptor potential (TRP) family, is gated by hypotonicity. Kinases WNK family influence expression and function thiazide-sensitive Na+-Cl- cotransporter, monogenic human hypertension has been linked to mutations in gene coding for WNK4. Along with isoforms are highly distal nephron. We show here that coexpression WNK4 downregulates TRPV4 embryonic kidney (HEK-293) cells this effect mediated via decreased cell surface...

10.1152/ajprenal.00391.2005 article EN AJP Renal Physiology 2006-01-11

The SLC30A8 gene codes for a pancreatic beta-cell-expressed zinc transporter, ZnT8. A polymorphism in the is associated with susceptibility to type 2 diabetes, although molecular mechanism through which this phenotype manifest incompletely understood. Such polymorphisms may exert their effect via impacting expression level of product. We used an shRNA-mediated approach reproducibly downregulate ZnT8 mRNA by >90% INS-1 beta cell line. ZnT8-downregulated cells exhibited diminished uptake...

10.1371/journal.pone.0005679 article EN cc-by PLoS ONE 2009-05-22

Intimal calcification is highly correlated with atherosclerotic plaque burden, but the underlying mechanism poorly understood. We recently reported that cartilage oligomeric matrix protein (COMP), a component of vascular extracellular matrix, an endogenous inhibitor smooth muscle cell calcification.To investigate whether COMP affects calcification.ApoE(-/-)COMP(-/-) mice fed chow diet for 12 months manifested more extensive in innominate arteries than did ApoE(-/-) mice. To which origins...

10.1161/circresaha.115.308021 article EN Circulation Research 2016-05-06
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