Intracellular heat shock protein 70: a possible therapeutic target for preventing postoperative atrial fibrillation

Postoperative atrial fibrillation is a frequent complication after cardiac surgery, associated with an increased risk of mortality and morbidity; thus, additional treatment and increasing costs of postoperative care are required. Inflammation and oxidative stress caused by ischemia-reperfusion during cardiac surgery may play an important role in the pathogenesis of postoperative atrial fibrillation. Stress-inducible heat shock proteins act as molecular chaperones that maintain cell homeostasis against stress in these events. Heat shock protein 70, the 70-kDa family of heat shock proteins, has been shown to closely associate with the incidence of postoperative atrial fibrillation in patients undergoing cardiac surgery. Extracellular heat shock protein 70 may be pro-inflammatory in the myocardial innate immune response caused by ischemia-reperfusion. In contrast, intracellular heat shock protein 70 exerts primarily anti-inflammatory and anti-apoptotic effects by preventing response to inflammatory cytokines, and inhibiting the nuclear factor Kappa B signaling pathway and different stages of mitochondrial-dependent pathways. Furthermore, the intracellular molecule can inhibit the induction and the maintenance of atrial fibrillation by attenuating Ca2+ overload in injuried myocardial cells. It is the intracellular heat shock protein 70, but not the extracellular molecule that holds as a therapeutic strategy for preventing postoperative atrial fibrillation.