Apoptosis, a form of cell death, is a regulatory process which is important for normal development but also plays a key role in skeletal muscle cell loss. This leads to degenerative pathologies such as sarcopenia which are caused by decreased levels of estrogens. 17β-Estradiol (E2) has been shown to exert survival actions in skeletal muscle cells; however, the molecular mechanisms by which the hormone protects cells from apoptosis are poorly understood.

In their recent study, Ronda et al. show that extracellular regulated kinase (ERK) and p38 mitogen-activated protein kinases (p38 MAPKs) play a role in mediating the protective effects of E2 in apoptosis. When inhibitors of ERK and p38 MAPK were present, H2O2-induced apoptosis was not prevented by E2, leading to alterations in the intracellular distribution of the murine C2C12 skeletal cell line which are typical of apoptosis. Ronda et al. (2010) Journal of Endocrinology 206, 235-246.

Read full article at DOI:10.1677/JOE-09-0429