B
Bao Wei Wang
Researcher at Fu Jen Catholic University
Publications - 11
Citations - 338
Bao Wei Wang is an academic researcher from Fu Jen Catholic University. The author has contributed to research in topics: Myocyte & Cardiac fibrosis. The author has an hindex of 10, co-authored 11 publications receiving 320 citations. Previous affiliations of Bao Wei Wang include Memorial Hospital of South Bend.
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MicroRNA-208a Increases Myocardial Fibrosis via Endoglin in Volume Overloading Heart
TL;DR: Investigation of the mechanism of regulation of mir-208a and endoglin in volume overload-induced heart failure found that treatment with atorvastatin can attenuate the myocardial fibrosis induced by volume overload through inhibition ofendoglin expression.
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Mechanical stretch enhances the expression of resistin gene in cultured cardiomyocytes via tumor necrosis factor-α
TL;DR: In conclusion, cyclic mechanical stretch enhances resistin expression in cultured rat neonatal cardiomyocytes, and the stretch-induced resistin is mediated by TNF-alpha, at least in part, through ERK MAP kinase and NF-kappaB pathways.
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Mechanical stretch via transforming growth factor-β1 activates microRNA208a to regulate endoglin expression in cultured rat cardiac myoblasts.
Kou-Gi Shyu,Bao Wei Wang,Bao Wei Wang,Gong-Jhe Wu,Gong-Jhe Wu,Chiu Mei Lin,Chiu Mei Lin,Hang Chang,Hang Chang +8 more
TL;DR: This data indicates that suppression of miR208a in cardiac cells by mechanical stress results in down-regulation in the expression of the genes involved in cardiac hypertrophy and fibrosis.
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Mechanism of the inhibitory effect of atorvastatin on endoglin expression induced by transforming growth factor‐β1 in cultured cardiac fibroblasts
TL;DR: The molecular mechanisms of atorvastatin on endoglin expression after TGF‐β1 stimulation in cardiac fibroblasts are investigated to investigate the mechanisms behind the inhibition of statins in patients with cardiac fibrosis.
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Cyclic stretch enhances the expression of Toll-like Receptor 4 gene in cultured cardiomyocytes via p38 MAP kinase and NF-κB pathway
TL;DR: The stretch-induced TLR4 is mediated through activation of p38 MAP kinase and NF-κB pathways and up-regulation by cyclic stretch increases monocyte adherence.