The myocardial ischemia occurs when the blood supply of coronary artery cannot meet the energy needs of myocardium .Certain time and certain extentischmia can give rise to cell injury.Reperfusion is the essential meas...The myocardial ischemia occurs when the blood supply of coronary artery cannot meet the energy needs of myocardium .Certain time and certain extentischmia can give rise to cell injury.Reperfusion is the essential measure to preventthe injury,but it was found recently that reperfusion could aggravate the injury.The pathogeny mechanism of ischemia- reperfusion(I- RI) injury remains incompletely elucidated.The thesis summarize the mechanism of I- RI only from calcium overload.展开更多
Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial in...Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction.展开更多
文摘The myocardial ischemia occurs when the blood supply of coronary artery cannot meet the energy needs of myocardium .Certain time and certain extentischmia can give rise to cell injury.Reperfusion is the essential measure to preventthe injury,but it was found recently that reperfusion could aggravate the injury.The pathogeny mechanism of ischemia- reperfusion(I- RI) injury remains incompletely elucidated.The thesis summarize the mechanism of I- RI only from calcium overload.
文摘Calpains are ubiquitous non-lysosomal Ca2+-dependent cysteine proteases also present in myocardial cytosol and mitochondria.Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia,reperfusion and postischemic structural remodelling.The increasing Ca2+-content and Ca2+-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains.Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria.Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria.Calpain inhibition can prevent or attenuate myocardial injury during ischemia,reperfusion,and in later stages of myocardial infarction.
