Abstract
The beneficial effects of oxytocin on infarct size and functional recovery of the ischemic reperfused heart are well documented. The mechanisms for this cardioprotection are not well defined. Evidence indicates that oxytocin treatment improves cardiac work, reduces apoptosis and inflammation, and increases scar vascularization. Oxytocin-mediated cytoprotection involves the production of cGMP stimulated by local release of atrial natriuretic peptide and synthesis of nitric oxide. Treatment with oxytocin reduces the expression of proinflammatory cytokines and reduces immune cell infiltration. Oxytocin also stimulates differentiation stem cells to cardiomyocyte lineages as well as generation of endothelial and smooth muscle cells, promoting angiogenesis. The beneficial actions of oxytocin may include the increase in glucose uptake by cardiomyocytes, reduction in cardiomyocyte hypertrophy, decrease in oxidative stress, and mitochondrial protection of several cell types. In cardiac and cellular models of ischemia and reperfusion, acute administration of oxytocin at the onset of reperfusion enhances cardiomyocyte viability and function by activating Pi3K and Akt phosphorylation and downstream cellular signaling. Reperfusion injury salvage kinase and signal transducer and activator of transcription proteins cardioprotective pathways are involved. Oxytocin is cardioprotective by reducing the inflammatory response and improving cardiovascular and metabolic function. Because of its pleiotropic nature, this peptide demonstrates a clear potential for the treatment of cardiovascular pathologies. In this review, we discuss the possible cellular mechanisms of action of oxytocin involved in cardioprotection.
Highlights
Specialty section: This article was submitted to Psychology for Clinical Settings, a section of the journal Frontiers in Psychology
Our studies have demonstrated that the expression of OT, OT receptor (OTR), Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and eNOS is reduced by more than 50% in hearts from db/db mice compared with lean wild-type control mice (Gutkowska et al, 2009)
We found that treatment of the D3 stem cell line with OT resulted in an increase in connexin 43 protein (Gassanov et al, 2008), and recent observations suggest a beneficial role of mitochondrial connexin 43 in postconditioning-induced reactive oxygen species (ROS) signaling, the precise function is not clear (Pagliaro et al, 2018)
Summary
Reviewed by: Robert Lukowski, University of Tübingen, Germany Pasquale Pagliaro, University of Turin, Italy. The beneficial effects of oxytocin on infarct size and functional recovery of the ischemic reperfused heart are well documented. The mechanisms for this cardioprotection are not well defined. Evidence indicates that oxytocin treatment improves cardiac work, reduces apoptosis and inflammation, and increases scar vascularization. The beneficial actions of oxytocin may include the increase in glucose uptake by cardiomyocytes, reduction in cardiomyocyte hypertrophy, decrease in oxidative stress, and mitochondrial protection of several cell types. Oxytocin is cardioprotective by reducing the inflammatory response and improving cardiovascular and metabolic function. We discuss the possible cellular mechanisms of action of oxytocin involved in cardioprotection
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