Angiotensin-converting enzyme inhibitor works as a scar formation inhibitor by down-regulating Smad and TGF-β-activated kinase 1 (TAK1) pathways in mice

British Journal of Pharmacology
Wei-Qiang TanKenneth E Bernstein

Abstract

Angiotensin-converting enzyme (ACE), an important part of the renin-angiotensin system, is implicated in stimulating the fibrotic processes in the heart, lung, liver and kidney, while an ACE inhibitor (ACEI) promotes physiological tissue repair in these organs. The mechanism is closely related to TGF-β1 pathways. However, the reported effects of applying ACEIs during scar formation are unclear. Hence, we explored the anti-fibrotic effects of an ACEI and the molecular mechanisms involved in a mouse scar model. After a full-thickness skin wound operation, ACE wild-type mice were randomly assigned to receive either ramipril, losartan or hydralazine p.o. ACE knockout (KO) mice and negative control mice only received vehicle (water). Wound/scar widths during wound healing and histological examinations were recorded at the final day. The ability of ACEI to reduce fibrosis via TGF-β1 signalling was evaluated in vitro and in vivo. ACE KO mice and mice that received ramipril showed narrower wound/scar width, reduced fibroblast proliferation, decreased collagen and TGF-β1 expression. ACEI attenuated the phosphorylation of small mothers against decapentaplegic (Smad2/3) and TGF-β-activated kinase 1 (TAK1) both in vitro and in vivo. The ex...Continue Reading

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Citations

Aug 7, 2019·Plastic and Reconstructive Surgery·Amanda MurphyMichael Bezuhly
Jul 18, 2020·Experimental Dermatology·Keshvad HedayatyanfardAhmad-Reza Dehpour
Jul 23, 2020·Experimental Dermatology·Igor Maciel Souza SilvaUlrike Muscha Steckelings
May 19, 2020·Matrix Biology : Journal of the International Society for Matrix Biology·Mohammad AlQudahMichael P Czubryt
Jun 17, 2020·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Tao ZhangWei-Qiang Tan

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