δ-Opioid Receptor as a Molecular Target for Increasing Cardiac Resistance to Reperfusion in Drug Development.
Natalia V NaryzhnayaAlexander V MukhomedzyanovMaria SirotinaLeonid N MaslovBoris K KurbatovAlexander S GorbunovMikhail KilinArtur KanAndrey V KrylatovYuri K PodoksenovSergey V LogvinovPublished in: Biomedicines (2023)
An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ 2 -opioid receptor (δ 2 -OR) increases the cardiac tolerance to reperfusion. It has been found that this δ 2 -OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ 2 -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 K ATP channels and the MPT pore.
Keyphrases
- acute myocardial infarction
- chronic pain
- pain management
- cerebral ischemia
- left ventricular
- acute ischemic stroke
- signaling pathway
- heart failure
- binding protein
- randomized controlled trial
- electronic health record
- blood brain barrier
- subarachnoid hemorrhage
- big data
- pi k akt
- single cell
- gene expression
- machine learning
- deep learning
- protein kinase