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Rongqi Wang

Researcher at Cardiovascular Institute of the South

Publications -  10
Citations -  1004

Rongqi Wang is an academic researcher from Cardiovascular Institute of the South. The author has contributed to research in topics: Apoptosis & Angiotensin II. The author has an hindex of 9, co-authored 9 publications receiving 968 citations. Previous affiliations of Rongqi Wang include Northwestern University.

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Journal ArticleDOI

Abrogation of bleomycin-induced epithelial apoptosis and lung fibrosis by captopril or by a caspase inhibitor.

TL;DR: The data suggest that the efficacy of captopril to inhibit experimental lung fibrogenesis is related to inhibition of apoptosis and the antifibrotic potential of a caspase inhibitor is demonstrated.
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Angiotensin II induces apoptosis in human and rat alveolar epithelial cells

TL;DR: The presence of a functional ANG II-dependent pathway for apoptosis in human and rat AECs is demonstrated and a role for the ANG II receptor and ACE in the induction of AEC apoptosis is suggested in vivo.
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Fas-induced apoptosis of alveolar epithelial cells requires ANG II generation and receptor interaction.

TL;DR: The data indicate that the induction of AEC apoptosis by Fas requires a functional renin-angiotensin system in the target cell and suggest that therapeutic control of A EC apoptosis is feasible through pharmacological manipulation of the local ren in-angiotsin system.
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Apoptosis of lung epithelial cells in response to TNF-alpha requires angiotensin II generation de novo.

TL;DR: Data indicate that the induction of A EC apoptosis by TNF‐α requires a functional renin/angiotensin system (RAS) in the target cell and suggest that therapeutic control of AEC apoptosis in response to TNF-α is feasible through pharmacologic manipulation of the local RAS.
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Angiotensin receptor subtype AT1 mediates alveolar epithelial cell apoptosis in response to ANG II

TL;DR: Data indicate that AEC apoptosis in response to ANG II is mediated by receptor subtype AT(1), despite the expression of mRNAs for both AT( 1) and AT(2).