Mechanisms of Myocardial ischemia–reperfusion Injury and the Cytoprotective Role of Minocycline: Scope and Limitations

Abstract

Deep insight into the complex mechanisms of myocardial ischemia-reperfusion injury has been attained in the past years. Minocycline is a second-generation tetracycline with US FDA approval for clinical use in various infections. Lately, several noninfectious cytoprotective activities of minocycline have been discovered as well. There now exists encouraging evidence of its protective role in cardiovascular pathology and its activity against myocardial ischemia-reperfusion injury. In this article, an overview of the major mechanisms involved in myocardial ischemia-reperfusion injury is presented. This is followed by an analysis of the mechanisms by which minocycline exerts its cytoprotective role and of studies that have been conducted in order to analyze minocycline, along with a review of the scope and limitations of its role as a cytoprotective agent.

Illuminating drug action by network integration of disease genes: a case study of myocardial infarction

“…Recent studies suggest that the combination of minocycline and aspirin prevents worsening of acute MI in diabetic rats by inhibiting MMP2 and MMP9 36 . In addition, encouraging evidence exists for minocycline’s protective role in cardiovascular pathology and its activity against myocardial ischemia-reperfusion injury 37 . Ginseng has been used as one of the traditional Chinese medicines for treating a variety of disorders.…”

MicroRNA-93 inhibits ischemia-reperfusion induced cardiomyocyte apoptosis by targeting PTEN

“…Myocardial ischemia/ reperfusion (I/R) injury contributes to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery or circulatory arrest, which represents a major cause of morbidity and mortality in humans with coronary heart disease. The molecular mechanisms underlying myocardial I/R injury, however, are complex, including oxidative stress, intracellular Ca 2+ overload, rapid restoration of physiological pH upon reperfusion, the mitochondrial permeability transition pore, and exaggerated inflammation [ 1 ].…”

miR-613 suppresses ischemia-reperfusion-induced cardiomyocyte apoptosis by targeting the programmed cell death 10 gene

“…I/R injury causes local myocardial inflammation and apoptosis, resulting in irreversible damage to the myocardium (1). Several mechanisms underlying myocardial I/R injury have been elucidated, including formation of oxygen free radicals, intracellular Ca + overload, neutrophil activation, and vascular endothelium damage (2). However, the complete profile of molecular pathways associated with myocardial I/R injury is not yet fully understood.…”