Scholarlink

<p>Connexin 43 (Cx43) is the principal connexin isoform expressed in the ventricular myocardium, where it is critically involved in the pathophysiology of cardiac ischemia–reperfusion injury. Its functions in this pathological condition span at least three different fronts. First, Cx43-mediated gap junctional channels contribute to the spread of cellular damage during reperfusion, allowing the transfer of sodium ions between injured and surviving cardiomyocytes. Further, under ischemic conditions, unapposed Cx43 hemichannels exacerbate injury by promoting calcium overload, metabolite losses, and membrane potential instability. Additionally, recent evidence suggest that mitochondrial Cx43 influences oxidative stress by modulating reactive oxygen species generation through the regulation of reverse electron transfer (RET) at the mitochondrial electron transport chain. These detrimental roles of Cx43 in acute myocardial ischemia–reperfusion injury, together with its previously described involvement in ischemic preconditioning, emphasize the dual functionality and importance of Cx43 in the context of acute myocardial infarction. The scope of this review is to summarize the current knowledge on the different mechanisms by which Cx43 promotes cell damage during myocardial infarction, with special emphasis on the regulation of RET.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Involvement of connexin 43 in myocardial ischemia–reperfusion injury

  • 期刊论文

  • 发表日期：

    2025年6月19日

查看全文
  • Marisol Ruiz-Meana,
  • Javier Inserte,
  • Marta Consegal,
  • Antonio Rodríguez-Sinovas

摘要

Connexin 43 (Cx43) is the principal connexin isoform expressed in the ventricular myocardium, where it is critically involved in the pathophysiology of cardiac ischemia–reperfusion injury. Its functions in this pathological condition span at least three different fronts. First, Cx43-mediated gap junctional channels contribute to the spread of cellular damage during reperfusion, allowing the transfer of sodium ions between injured and surviving cardiomyocytes. Further, under ischemic conditions, unapposed Cx43 hemichannels exacerbate injury by promoting calcium overload, metabolite losses, and membrane potential instability. Additionally, recent evidence suggest that mitochondrial Cx43 influences oxidative stress by modulating reactive oxygen species generation through the regulation of reverse electron transfer (RET) at the mitochondrial electron transport chain. These detrimental roles of Cx43 in acute myocardial ischemia–reperfusion injury, together with its previously described involvement in ischemic preconditioning, emphasize the dual functionality and importance of Cx43 in the context of acute myocardial infarction. The scope of this review is to summarize the current knowledge on the different mechanisms by which Cx43 promotes cell damage during myocardial infarction, with special emphasis on the regulation of RET.