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Aerobic exercise involves in ameliorating kidney injury, but the underlying mechanisms are not fully clarified. In this study, we elucidated the potential mechanisms of aerobic exercise in ameliorating kidney injury following myocardial infarction (MI). In vivo, wildtype and alcat1 knockout mice were used to establish the MI model, and subjected to six-week moderate-intensity aerobic exercise. In vitro, Normal Rat Kidney (NRK) cells treated with H2O2 and recombinant human Irisin (rhIrisin) were used for exploring potential mechanisms. Our results showed that Irisin expression was up-regulated by aerobic exercise in kidneys after MI, while ALCAT1 was reduced. In alcat1 knockout mice, we found that ALCAT1 involved in the progressions of oxidative stress and apoptosis in impaired kidney tissues of MI mice, but aerobic exercise reversed these changes. Furthermore, in vitro, we observed that Irisin inhibited both H2O2-treatment or overexpression of alcat1-induced oxidative stress and apoptosis in NRK cells, partially via AMPK-Sirt1-PGC-1α pathway. These findings reveal that aerobic exercise participates in alleviating the levels of oxidative stress and apoptosis in impaired kidney tissues following MI, partially via activating FNDC5/Irisin-AMPK-Sirt1-PGC-1α signaling pathway and inhibiting ALCAT1 expression.

Figure 1. AICAR, the AMPK agonist, accelerated the inhibited effect of rhIrisin on oxidative stress-induced apoptosis in NRK cells.

This study is aimed to explore the underlying mechanisms of the association between aerobic exercise and ameliorating kidney injury. In this study, the authors elucidated the potential mechanisms of aerobic exercise in ameliorating kidney injury following myocardial infarction (MI).These findings reveal that aerobic exercise participates in alleviating the levels of oxidative stress and apoptosis in impaired kidney tissues following MI, partially via activating FNDC5/Irisin-AMPK-Sirt1-PGC-1α signaling pathway and inhibiting ALCAT1 expression.

 
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