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Exercise training activates neuregulin 1/ErbB signaling and promotes cardiac repair in a rat myocardial infarction model. | LitMetric

AI Article Synopsis

  • Exercise training (ET) after a myocardial infarction (MI) was studied to see if it activates NRG1/ErbB signaling, which is important for heart repair and regeneration.
  • Male Sprague-Dawley rats underwent four weeks of ET, showing increased NRG1 expression and improved heart function, alongside enhanced cardiomyocyte proliferation and reduced cell death.
  • Blocking ErbB signaling with AG1478 decreased the benefits of ET, suggesting that ErbB activation is crucial for the positive effects of exercise on cardiac repair post-MI.

Article Abstract

Aims: Exercise training (ET) has a cardioprotective effect and can alter the molecular response to myocardial infarction (MI). The Neuregulin 1 (NRG1)/ErbB signaling plays a critical role in cardiac repair and regeneration in the failing heart. We sought to investigate whether ET following MI could activate the NRG1/ErbB signaling and promote cardiac repair and regeneration.

Main Methods: Male Sprague-Dawley rats were used to establish the MI model. Exercise-trained animals were subjected to four weeks of exercise (16m/min, 50min/d, 5d/wk) following the surgery. AG1478 was used as an inhibitor of ErbB (1mg/kg body weight, administered i.v. every other day during the process of training). NRG1/ErbB signaling activation, cardiomyocyte (CM) proliferation and apoptosis were evaluated.

Key Findings: In the exercise-trained rats, NRG1 expression was up-regulated and ErbB/PI3K/Akt signaling was activated compared with the MI group. In addition, ET preserved heart function accompanied with increased numbers of BrdU(+) CMs, PCNA(+) CMs and c-kit(+) cells, and reduced apoptosis level in the MI rats. In contrast, blocking ErbB signaling by AG1478 attenuated the ET-induced cardiac repair and regeneration.

Significance: ET up-regulates NRG1 expression and activates ErbB2, ErbB4 and PI3K/Akt signal transduction to promote cardiac repair through endogenous regeneration. Activation of ErbB may be an underlying mechanism for the ET-induced cardiac repair and regeneration following MI.

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Source
http://dx.doi.org/10.1016/j.lfs.2016.02.055DOI Listing

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