Key result
Connexin and nitric oxide signaling interplay drives cardiac protection and conditioning.
Mitochondrial connexins and nitric oxide signaling are essential components of myocardial adaptation to ischemia and represent potential therapeutic targets for cardioprotection.
Connexin-NO pathways merit no clinical targeting yet; leaves open mechanistic roles in cardioprotection for future targeted studies.
-nitrosation represents a regulatory molecular mechanism similar to phosphorylation and is essential for IPC. Unlike conditioning phenomena, the mechanistic basis of myocardial stunning and hibernation remains poorly understood. In this review article, we hypothesize that the disruption of electrical syncytium of the myocardium may underly myocardial stunning and hibernation. Considering that the connexins are the building blocks of gap junctions which represent primary structural basis of electrical syncytium, we discuss data on the involvement of connexins into myocardial conditioning, stunning, and hibernation. We also show how NO-mediated signaling is involved in myocardial stunning and hibernation. Connexins represent an essential element of adaptation phenomena of the heart at the level of both the cardio- myocytes and the mitochondria. Nitric oxide targets mitochondrial connexins which may affect electrical syncytium continuum in the heart. Mitochondrial connexins may play an essential role in NO-dependent mechanisms of myocardial adaptation to ischemia.
No takes yet. Share an insight, caveat, or question.
Shvedova et al. (2018) conducted a review in Myocardial ischemia and reperfusion injury. The interplay between connexins and nitric oxide-mediated signaling inside and outside mitochondria plays a pivotal role in cardiac protection and conditioning phenomena.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: