Abstract
Gap junctions are the main form of interaction between cardiomyocytes, through which the electrochemical activities between cardiomyocytes can be synchronized to maintain the normal function of the heart. Connexins are the basis of gap junctions. Changes in the expression, structural changes (e.g., phosphorylation and dephosphorylation), and distribution of connexins can affect the normal electrophysiological activities of the heart. Myocardial infarction (MI) and concurrent arrhythmia, shock, or heart failure can endanger life. The structural and functional damage of connexin (Cx) 43 in cardiomyocytes is a central part of the pathological progression of MI and is one of the main pathological mechanisms of arrhythmia after MI. Therefore, increasing Cx43 expression has become one of the main measures to prevent MI. Also, intervention in Cx43 expression can improve the structural and electrical remodeling of the myocardium to improve MI prognosis. Here, research progress of Cx43 in MI and its prevention and treatment using Traditional Chinese Medicine formulations is reviewed.
Highlights
Cxs are transmembrane proteins that assemble to form gap junctions (GJs) in vertebrate animals
Acute myocardial infarction (MI) is an acute and persistent myocardial necrosis caused by ischemia and hypoxia of coronary arteries that can be complicated with arrhythmia, shock, or heart failure and can often endanger life
MI often results in reduced Cx43 expression, increased lateral distribution, and altered phosphorylation status, whereas Cx43 regulates channel activity through phosphorylation/ dephosphorylation and nitroso modification
Summary
E interaction domain between Cx43 and CIP75 is located at multiple phosphorylation sites between Lys264 and Asn302 of the Py sequence (Figure 3). e UBL domain interacts with the S2/RPN1 and S5a/RPN10 protein subunits of the regulated 19S proteasome cap subunit of the 26S proteasome complex. A novel interactor of Cx43 in the heart, Eps homology domain protein-1, can interact with Cx43 through Eps to regulate its endocytic transport, thereby participating in the pathological remodeling of Cx43; reducing its expression, as well as phosphorylation and ubiquitination of Cx43, can promote this process [19]. Regardless of the specific etiology and organ localization, systemic inflammation rapidly causes atrial electrical remodeling by downregulating expression of cardiac Cxs through increased expression of interleukin (IL) 6. This process is short-lived, these changes can significantly increase the risk of atrial fibrillation and related complications during active inflammation [21].
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