The δ2-opioid receptor represents a potential molecular target for developing cardioprotective drugs against ischemia-reperfusion injury.
δ2-OR activation may enhance cardiomyocyte reperfusion tolerance; hypothesis-generating for clinical translation, should not change practice.
An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ2-opioid receptor (δ2-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ2-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ2-OR agonist deltorphin II depends on the activation of several protein kinases, including PKCδ, ERK1/2, PI3K, and PKG. Hypothetical end-effectors of the cardioprotective effect of deltorphin II are the sarcolemmal KATP channels and the MPT pore.
No takes yet. Share an insight, caveat, or question.
Naryzhnaya et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: