Abstract
Aging results in accumulation of extracellular matrix proteins and impairment of cardiac function. Oxidative stress is a potential mechanism in age‐associated cardiac fibrosis. We have previously show exercise training reduces fibrosis and expression of transforming growth factor‐beta (TGF‐ß1) in the aging heart, concomitant with a reduction in oxidative stress and upregulation of the manganese‐isoform of superoxide dismutase (MnSOD). However, the causal relationship between MnSOD and TGF‐ß1 in the aging heart is unknown. Thus, we tested the hypothesis that overexpression of Mn‐SOD would reduce TGF‐ß1 and markers of fibrosis in the aging heart. Old (27 mo) wild type (OWT) animals had larger cardiac myocyte cross‐sectional areas (CSA) that young (4 mo) wild type mice (YWT), an effect reduced in Old Mn‐SOD transgenic mice animals (Otg). TGF‐β1 and collagen I abundance was higher in OWT vs. YWT, while overexpression of MnSOD attenuated TGF‐β1 and collagen I in hearts of old mice. Matrix metalloproteinase‐9 (MMP‐9) was lower in OWT, with age dependent suppression of MMP‐9 prevented by Mn‐SOD. Results indicate that overexpression of Mn‐SOD overexpression protects against age‐related upregulation of TGF‐ß1 and fibrosis, suggestive that elevation of MnSOD with exercise training may indeed be cardioprotective against fibrosis and remodeling. Supported by AHA 0855158F; NIH AR054084
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