BACKGROUND: in the heart is unclear. OBJECTIVES: , mitochondrial function, and cardiac contractile function. METHODS: Cultured cardiac myocytes were subjected to different stresses in vitro. Mice were subjected to chronic pressure overload. Tissues and blood biomarkers were studied in patients with aortic stenosis. RESULTS: activation, which correlated with reduced tissue cardiomyocyte death and fibrosis and lower plasma levels of biomarkers of cardiac damage (high-sensitivity troponin T) and dysfunction (N-terminal pro-B-type natriuretic peptide). CONCLUSIONS: ameliorates mitochondrial and contractile dysfunction, suggesting that it may serve an important protective role in the stressed heart.
Smyrnias et al. (2019) studied this question.