Wei Kong

Summary

Affiliation: Peking University
Country: China

Publications

  1. He L, Fu Y, Deng J, Shen Y, Wang Y, Yu F, et al. Deficiency of FAM3D (Family With Sequence Similarity 3, Member D), A Novel Chemokine, Attenuates Neutrophil Recruitment and Ameliorates Abdominal Aortic Aneurysm Development. Arterioscler Thromb Vasc Biol. 2018;38:1616-1631 pubmed publisher
    ..FAM3D, as a dual agonist of FPR1 and FPR2, induced Mac-1-mediated neutrophil recruitment and aggravated AAA development through FPR-related Gi protein and ?-arrestin signaling. ..
  2. Wang Y, Chen D, Zhang Y, Wang P, Zheng C, Zhang S, et al. Novel Adipokine, FAM19A5, Inhibits Neointima Formation After Injury Through Sphingosine-1-Phosphate Receptor 2. Circulation. 2018;138:48-63 pubmed publisher
    ..Downregulation of FAM19A5 during obesity may trigger cardiometabolic diseases. ..
  3. Yu B, Liu Z, Fu Y, Wang Y, Zhang L, Cai Z, et al. CYLD Deubiquitinates Nicotinamide Adenine Dinucleotide Phosphate Oxidase 4 Contributing to Adventitial Remodeling. Arterioscler Thromb Vasc Biol. 2017;37:1698-1709 pubmed publisher
    ..These effects were abolished in CYLD-/- mice. CYLD contributes to the transdifferentiation of AFs via deubiquitinating Nox4 and may play a role in vascular remodeling. ..
  4. Sun W, Pang Y, Liu Z, Sun L, Liu B, Xu M, et al. Macrophage inflammasome mediates hyperhomocysteinemia-aggravated abdominal aortic aneurysm. J Mol Cell Cardiol. 2015;81:96-106 pubmed publisher
    ..Blocking mitochondrial ROS production in macrophages abolished inflammasome activation. Our study highlights the potential importance of macrophage inflammasome in the pathogenesis and development of HHcy-aggravated AAA. ..
  5. Jia Y, Wang M, Mao C, Yu F, Wang Y, Xiao R, et al. COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity. Cell Death Dis. 2018;9:676 pubmed publisher
    ..Maintaining the homeostasis of mitochondrial respiration through COMP-prohibitin 2 interaction may shed light on prevention of vascular disease. ..
  6. Ma B, Yao F, Xie N, Mao C, Liu F, Gong Z, et al. Cartilage oligomeric matrix protein is a novel notch ligand driving embryonic stem cell differentiation towards the smooth muscle lineage. J Mol Cell Cardiol. 2018;121:69-80 pubmed publisher
    ..In conclusion, COMP served as a potential ligand of Notch1, thereby driving ESC-VSMC differentiation. ..
  7. Yang N, Yu F, Shao G, Fu Y, Kong W. The E3 ubiquitin ligase c-Cbl mediates integrin ?1 ubiquitination during dilated cardiomyopathy. Biochem Biophys Res Commun. 2016;479:728-735 pubmed publisher
    ..In conclusion, our results demonstrate that c-Cbl mediates the ubiquitination/degradation of integrin ?1, which leads to COMP deficiency-induced DCM. ..
  8. request reprint
    Liu Y, Kong W. [The mechanisms of medial vascular calcification]. Sheng Li Xue Bao. 2016;68:592-610 pubmed
    ..Medial vascular calcification is a pathological phenomenon commonly existed in diabetes, chronic kidney failure and aging. The current review summarizes the mechanisms of medial vascular calcification. ..
  9. Li T, Yu B, Liu Z, Li J, Ma M, Wang Y, et al. Homocysteine directly interacts and activates the angiotensin II type I receptor to aggravate vascular injury. Nat Commun. 2018;9:11 pubmed publisher
    ..Together, these findings suggest that strategies aimed at blocking the AT1 receptor may mitigate HHcy-associated aneurysmal vascular injuries. ..

More Information

Publications15

  1. Li L, Zhao Q, Kong W. Extracellular matrix remodeling and cardiac fibrosis. Matrix Biol. 2018;68-69:490-506 pubmed publisher
    ..Understanding the comprehensive molecules and pathways involved in ECM homeostasis and remodeling may provide important novel potential targets for preventing and treating cardiac fibrosis. ..
  2. Kessler T, Zhang L, Liu Z, Yin X, Huang Y, Wang Y, et al. ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1. Circulation. 2015;131:1191-201 pubmed publisher
    ..Our study revealed a novel mechanism by which ADAMTS-7 affects neointima formation. Thus, ADAMTS-7 is a promising treatment target for postinjury vascular intima hyperplasia. ..
  3. Fu Y, Gao C, Liang Y, Wang M, Huang Y, Ma W, et al. Shift of Macrophage Phenotype Due to Cartilage Oligomeric Matrix Protein Deficiency Drives Atherosclerotic Calcification. Circ Res. 2016;119:261-76 pubmed publisher
    ..These results reveal that COMP deficiency acted via integrin ?3 to drive macrophages toward the atherogenic and osteogenic phenotype and thereby aggravate atherosclerotic calcification. ..
  4. Wang M, Fu Y, Gao C, Jia Y, Huang Y, Liu L, et al. Cartilage oligomeric matrix protein prevents vascular aging and vascular smooth muscle cells senescence. Biochem Biophys Res Commun. 2016;478:1006-13 pubmed publisher
    ..Taken together, these findings revealed the essential role of COMP in retarding the development of vascular aging and VSMC senescence. ..
  5. Yu H, Jia Q, Feng X, Chen H, Wang L, Ni X, et al. Hypoxia decrease expression of cartilage oligomeric matrix protein to promote phenotype switching of pulmonary arterial smooth muscle cells. Int J Biochem Cell Biol. 2017;91:37-44 pubmed publisher
    ..05). These data suggest that COMP could normally have a protective role against PASMC phenotype switching and maintain BMP2/BMPR2 signaling, and these protective actions could be lost as a result of hypoxia promoting a depletion of COMP. ..
  6. Zhao G, Fu Y, Cai Z, Yu F, Gong Z, Dai R, et al. Unspliced XBP1 Confers VSMC Homeostasis and Prevents Aortic Aneurysm Formation via FoxO4 Interaction. Circ Res. 2017;121:1331-1345 pubmed publisher
    ..Our study revealed the pivotal role of the XBP1u-FoxO4-myocardin axis in maintaining the VSMC contractile phenotype and providing protection from aortic aneurysm formation. ..