Is autophagy upregulated in ovarian endometriosis : a possible interplay with p53 and heme oxygenase-1?
The upregulated autophagic process observed in ovarian endometriomas can be regarded as an integral part of endometriosis pathogenesis, possibly contributing to survival of endometriotic cells in ectopic sites and to lesion maintenance. The decreased susceptibility to apoptosis and the persistent oxidative stress experienced by endometriotic cells could favor autophagy stimulation.
Familial concordance for Na+/H+ antiport activity in long-term cultured skin fibroblasts from type 1 diabetic siblings suggests that at least some of the in vitro phenotypical characteristics of these cells are likely to be genetically determined and to be, at least in part, independent of in vivo metabolic control.