Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines.

ABSTRACT: Myocardial tissue homeostasis is critically important for heart development, growth and function throughout the life course. The loss of cardiomyocytes under pathological conditions ultimately leads to cardiovascular disease due to the limited regenerative capacity of the postnatal mammalian heart. Inhibition of electron transport along the mitochondrial respiratory chain causes cellular stress characterized by ATP depletion as well as excessive generation of reactive oxygen species. Adult cardiomyocytes are highly susceptible to mitochondrial dysfunction whereas embryonic cardiomyocytes in the mouse heart have been shown to be resistant towards mitochondrial complex III inhibition. To functionally characterize the molecular mechanisms mediating this stress tolerance, we used H9c2 cells as

SUBMITTER: Grun B 

PROVIDER: S-EPMC9538794 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature