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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocin is a mammalian hormone that is released mainly after distension of the uterine cervix. In this study, we report that oxytocin stimulates intracellular release of calcium, and also activates AMPK (AMP-activated protein kinase) in C2C12 myoblast cells in a time/dose-dependent manner. Oxytocin receptor mRNA was detected in C2C12 cells. In addition, oxytocin stimulated glucose uptake and, moreover, inhibition of either CaMKK (Ca(2+)/calmodulin-dependent protein kinase kinase) or AMPK blocked oxytocin-mediated AMPK activation and glucose uptake. Taken together, our findings suggest that oxytocin may serve a peripheral metabolic function in skeletal muscle cells through the calcium-CaMKK-AMPK pathway.
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PMID:Oxytocin stimulates glucose uptake in skeletal muscle cells through the calcium-CaMKK-AMPK pathway. 1855 43

Coronary artery disease (CAD) is a major cardiovascular disease responsible for high morbidity and mortality worldwide. The major pathophysiological basis of CAD is atherosclerosis in association with varieties of immunometabolic disorders that can suppress oxytocin (OT) receptor (OTR) signaling in the cardiovascular system (CVS). By contrast, OT not only maintains cardiovascular integrity but also has the potential to suppress and even reverse atherosclerotic alterations and CAD. These protective effects of OT are associated with its protection of the heart and blood vessels from immunometabolic injuries and the resultant inflammation and apoptosis through both peripheral and central approaches. As a result, OT can decelerate the progression of atherosclerosis and facilitate the recovery of CVS from these injuries. At the cellular level, the protective effect of OT on CVS involves a broad array of OTR signaling events. These signals mainly belong to the reperfusion injury salvage kinase pathway that is composed of phosphatidylinositol 3-kinase-Akt-endothelial nitric oxide synthase cascades and extracellular signal-regulated protein kinase 1/2. Additionally, AMP-activated protein kinase, Ca2+/calmodulin-dependent protein kinase signaling and many others are also implicated in OTR signaling in the CVS protection. These signaling events interact coordinately at many levels to suppress the production of inflammatory cytokines and the activation of apoptotic pathways. A particular target of these signaling events is endoplasmic reticulum (ER) stress and mitochondrial oxidative stress that interact through mitochondria-associated ER membrane. In contrast to these protective effects and machineries, rare but serious cardiovascular disturbances were also reported in labor induction and animal studies including hypotension, reflexive tachycardia, coronary spasm or thrombosis and allergy. Here, we review our current understanding of the protective effect of OT against varieties of atherosclerotic etiologies as well as the approaches and underlying mechanisms of these effects. Moreover, potential cardiovascular disturbances following OT application are also discussed to avoid unwanted effects in clinical trials of OT usages.
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PMID:Therapeutic Potential of Oxytocin in Atherosclerotic Cardiovascular Disease: Mechanisms and Signaling Pathways. 3117 79

Based on the ancient role of oxytocin and its homologues as amplifiers of reproduction we argue for an evolutionary coupling of oxytocin to signaling pathway which support restorative mechanisms of cells and tissue. In particular, the survival and function of different categories of stem cells and primordial cells are enhanced by mitogen-activated protein kinase (MAPK) pathways. Furthermore, oxytocin stimulates the AMP-activated protein kinase pathway (AMPK) in numerous of cell types which promotes the maintenance of different cell structures. This involves autophagic processes and, in particular, may support the renewal of mitochondria. Mitochondrial fitness may protect against oxidative and inflammatory stress - a well-documented effect of oxytocin. The combined specific trophic and protective effects oxytocin may delay several degenerative phenomena including sarcopenia, type-2 diabetes and atherosclerosis. These effects may be exerted both on a central level supporting the function and integrity of the hypothalamus and peripherally acting directly on blood vessels, pancreas, heart, skeletal muscles and adipose tissue etc. Furthermore, in the capacity of being both a hormone and neuromodulator, oxytocin interacts with numerous of regulatory mechanisms particularly the autonomic nervous system and HPA-axis which may reduce blood pressure and affect the immune function. The potential of the oxytocin system as a behavioral and molecular target for the prevention and treatment of cardiovascular disease is discussed. Focus is put on the affiliative and sexual significance and the different options and limitations associated with a pharmaceutical approach. MeSH: Aging, Atherosclerosis, Heart, Hypothalamus, Inflammation, Love, Orgasm, Oxytocin.
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PMID:Oxytocin may have a therapeutical potential against cardiovascular disease. Possible pharmaceutical and behavioral approaches. 3203 12