Molecular mechanisms underlying oxytocin-induced cardiomyocyte protection from simulated ischemia–reperfusion

  title={Molecular mechanisms underlying oxytocin-induced cardiomyocyte protection from simulated ischemia–reperfusion},
  author={Araceli Gonzalez-Reyes and Ahmed M{\'e}naouar and Denis Yip and Bogdan Alexandru Danalache and Marek Jankowski},
  journal={Molecular and Cellular Endocrinology},

The Role of Oxytocin in Cardiovascular Protection

Evidence indicates that oxytocin treatment improves cardiac work, reduces apoptosis and inflammation, and increases scar vascularization, as well as cardioprotection, by reducing the inflammatory response and improving cardiovascular and metabolic function.

Oxytocin maintains lung histological and functional integrity to confer protection in heat stroke

The data indicate that OT pretreatment can reduce the ischemic, inflammatory and oxidative responses related to heat-induced ALI in rats.

Oxytocin and cardioprotection in diabetes and obesity

It is shown that chronic OT treatment prevents the development of diabetic cardiomyopathy in the db/db mouse and may help replace lost CMs by stimulating the in situ differentiation of cardiac stem cells into functional mature CMs.

Oxytocin-induced endothelial nitric oxide dependent vasorelaxation and ERK1/2-mediated vasoconstriction in the rat aorta

Oxytocin stimulation of PI3K/eNOS-derived nitric oxide may participate in maintenance of cardiovascular homeostasis, and different vascular reactivities to low or high dose of oxytocin suggest that Oxytocin may have different regulatory effects on vascular tone under physiological or pathophysiological conditions.



Oxytocin exerts protective effects on in vitro myocardial injury induced by ischemia and reperfusion.

The data suggest that the negative chronotropic action of oxytocin participates in its protective effects on ischemia-reperfusion-induced myocardial injury, and demonstrates an attenuation of the infarct size in oxytocIn-treated hearts, indicating a cardioprotective effect of Oxytocin.

Prolonged oxytocin treatment in rats affects intracellular signaling and induces myocardial protection against infarction.

Positive effects of oxytocin that may ameliorate negative consequences of stress on the heart are, at least in part, mediated through p38-MAPK and Akt kinase pathways.

Redox regulation of ischemic preconditioning is mediated by the differential activation of caveolins and their association with eNOS and GLUT-4.

A novel redox mechanism in IP-induced eNOS and GLUT-4 translocation and the role of caveolar paradox in making the heart euglycemic during the process of ischemia, leading to myocardial protection in a clinically relevant rat ischemic model is demonstrated.

Anti-inflammatory effect of oxytocin in rat myocardial infarction

Results indicate that continuous OT delivery reduces inflammation and apoptosis in infarcted and remote myocardium, thus improving function in the injured heart.

Postinfarct Treatment With Oxytocin Improves Cardiac Function and Remodeling via Activating Cell-survival Signals and Angiogenesis

Postinfarct treatment with OT reduces myocardial infarct size and improves LV function and remodeling by activating OT receptors and prosurvival signals and by exerting antifibrotic and angiogenic effects through activation of MMP-1, endothelial NO synthase, and vascular endothelial growth factor.