期刊
AGING-US
卷 14, 期 10, 页码 4390-4401出版社
IMPACT JOURNALS LLC
关键词
myocardial fibrosis; hypertension; treadmill training; aging
资金
- Ministry of Science and Technology [MOST 110-2410-H-227-001, MOST 110-2314-B-468 -004]
- National Taipei University of Nursing and Health Science, Taiwan
- University of Taipei
- China Medical University
- Wei-fang Medical University, China
Exercise training reduces cardiac fibrosis in early aged hypertensive rats by decreasing fibrotic-related protein levels and suppressing fibrotic pathways, providing a new therapeutic approach for preventing adverse cardiac fibrosis and myocardial abnormalities.
Background: An inappropriate accumulation of fibrillar collagen is a common pathologic feature of early aged hypertensive heart disease, but little information regarding the effects of exercise training on cardiac fibrosis in hypertension is available. The purpose of this study was to evaluate the effects of exercise training on cardiac fibrotic pathways in early aged hypertensive rats. Methods: Masson's trichrome staining and Western blotting were performed on the excised left ventricle from twenty male spontaneously hypertensive rats at age of 48 weeks, which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on a treadmill running occurred 5 days/week for 60 min/day, for 12 weeks), and from age-matched male Wistar-Kyoto normotensive controls (WKY). Results: Interstitial fibrosis was reduced in the SHR-Ex group when compared with the SHR group. The fibrotic-related protein levels of AT(1)R, FGF23, LOX-2, TGF-beta, CTGF, p-Smad 2/3, MMP-2/TIMP-2, MMP-9/TIMP-1, uPA and collagen I were decreased in the SHR-EX group, when compared with the SHR group. Conclusions: Exercise training suppresses early aged hypertensive heart-induced LOX-2/TGF-beta-mediated fibrotic pathways associated with decreasing AT1R and FGF23, which might provide a new therapeutic effect for exercise training to prevent adverse cardiac fibrosis and myocardial abnormalities in early aged hypertension.
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