Exercise training attenuates age-dependent elevation of angiotensin II type 1 receptor and Nox2 signaling in the rat heart
- Authors
- Lee, Yang; Kwak, Hyo-Bum; Hord, Jeff; Kim, Jong-Hee; Lawler, John M.
- Issue Date
- Oct-2015
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- Aging; Heart; Angiotensin II receptor 1; NADPH oxidase; TGF-beta
- Citation
- EXPERIMENTAL GERONTOLOGY, v.70, pp.163 - 173
- Indexed
- SCIE
SCOPUS
- Journal Title
- EXPERIMENTAL GERONTOLOGY
- Volume
- 70
- Start Page
- 163
- End Page
- 173
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/156258
- DOI
- 10.1016/j.exger.2015.07.016
- ISSN
- 0531-5565
- Abstract
- Fibrosis of the aging heart impedes cardiac function and increases the risk of arrhythmias and heart disease. Previously, we demonstrated that exercise-induced reduction of collagen I in the aging heart was linked to a suppression of oxidative stress and transforming growth factor-beta (TGF-beta). The renin-angiotensin II system (RAS) increases oxidative stress via NADPH oxidase-2 (Nox2) and thus elevates TGF-beta and collagen accumulation. Therefore, we tested the hypothesis that exercise training would alleviate age-related upregulation of the angiotensin II receptor I (AT1R) and NADPH oxidase-2 (Nox2), concomitant with suppression of TGF-beta and fibrosis. Young (3 months, n = 20) and old (31 months, n = 20) Fischer 344 x Brown Norway F1 (FBNF1) hybrid rats were assigned into sedentary and exercise groups, with exercise training rats training on a treadmill 45 min/day, 5 days/week for the next 12 weeks. Exercise training mitigated age-related upregulation of AT1R, Nox2 activity, and Nox2 subunits gp91phox and p47phox. Exercise training also attenuated TGF-beta positive staining and downstream effectors of fibrosis in the aging heart: connective tissue growth factor, phosphorylation of Smad2 at Ser423, myofibroblast proliferation, and collagen I-positive staining. Our results are consistent with the hypothesis that exercise training protects against age-dependent cardiac fibrosis by suppressing AT1R and Nox2 as part of a RAS-Nox2-TGF-beta pathway.
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