PGC-1alpha over-expression promotes recovery from mitochondrial dysfunction and cell injury.

摘要: Cell death from mitochondrial dysfunction and compromised bioenergetics is common after ischemia-reperfusion injury toxicant exposure. Thus, promoting biogenesis therapeutically attractive for sustaining oxidative phosphorylation maintaining ATP-dependent cellular functions. Here, we evaluated increased prior to or oxidant exposure in primary cultures of renal proximal tubular cells (RPTC). Over-expression the regulator PPAR-gamma cofactor-1 alpha (PGC-1alpha) control RTPC basal uncoupled respiration, ATP, mitochondria. Increasing number/function did not preserve function, but potentiated cell death. However, accelerated recovery function. In treated RPTC, protein expression was reduced by 50%. Also, ATP respiration decreased 48 h exposure, whereas function injured RPTC over-expressing PGC-1alpha returned values. up-regulation accelerates