Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. Over the last 30 years, the development of advanced coronary care, implementation of early reperfusion strategies, and introduction of new pharmacologic approaches have greatly reduced mortality during the first 30 days after acute myocardial infarction. However, improved survival during the acute events resulted in the expansion of the pool of patients at risk for the development of heart failure. Ischemia or Ischemia-reperfusion induces myocardial injury including necrosis, immune response and apoptosis, and subsequent cardiac fibrosis, which reduces cardiac contractility and results in heart failure. Activation of pro-inflammatory signaling pathways, complement cascade, NF-?B system, and cytokine signaling has been involved in ischemic myocardial injury. Although experimental evidence supports that activation of endogenous cardioprotective properties could prevent the development of heart failure, detailed molecular mechanisms of myocardial injury or protection need to be clarified systemically.
Owing to the high socioeconomic burden of acute myocardial infarction and its chronic consequences in surviving patients, understanding the pathophysiology of cardiac injury is a major priority for cardiovascular research. This Research Topic will bring together a comprehensive discussion on the pathophysiologic basis of ischemic myocardial injury, the endogenous mechanisms of cardiac repair, and the pathways involved in post-infarction remodeling or some biomarker for the adverse outcome of patients with ischemic heart diseases.
We welcome basic research and clinical studies on the following aspects:
1) Novel molecular signals mediating apoptotic death in ischemic cardiomyocytes.
2) Novel molecular mechanisms about the regulation of the fate of noncardiomyocytes in the ischemic heart.
3) The interaction among various cardiac cells in ischemic heart.
4) Novel molecular mechanisms in cardiac repair following myocardial infarction.
5) Identification of biomarkers for predicting adverse outcome in patients with ischemic heart diseases.
Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. Over the last 30 years, the development of advanced coronary care, implementation of early reperfusion strategies, and introduction of new pharmacologic approaches have greatly reduced mortality during the first 30 days after acute myocardial infarction. However, improved survival during the acute events resulted in the expansion of the pool of patients at risk for the development of heart failure. Ischemia or Ischemia-reperfusion induces myocardial injury including necrosis, immune response and apoptosis, and subsequent cardiac fibrosis, which reduces cardiac contractility and results in heart failure. Activation of pro-inflammatory signaling pathways, complement cascade, NF-?B system, and cytokine signaling has been involved in ischemic myocardial injury. Although experimental evidence supports that activation of endogenous cardioprotective properties could prevent the development of heart failure, detailed molecular mechanisms of myocardial injury or protection need to be clarified systemically.
Owing to the high socioeconomic burden of acute myocardial infarction and its chronic consequences in surviving patients, understanding the pathophysiology of cardiac injury is a major priority for cardiovascular research. This Research Topic will bring together a comprehensive discussion on the pathophysiologic basis of ischemic myocardial injury, the endogenous mechanisms of cardiac repair, and the pathways involved in post-infarction remodeling or some biomarker for the adverse outcome of patients with ischemic heart diseases.
We welcome basic research and clinical studies on the following aspects:
1) Novel molecular signals mediating apoptotic death in ischemic cardiomyocytes.
2) Novel molecular mechanisms about the regulation of the fate of noncardiomyocytes in the ischemic heart.
3) The interaction among various cardiac cells in ischemic heart.
4) Novel molecular mechanisms in cardiac repair following myocardial infarction.
5) Identification of biomarkers for predicting adverse outcome in patients with ischemic heart diseases.
