Myocardial infarction Caspases

Zidar N, Dolenc-Strazar Z, Jeruc J, Stajer D. Immunohistochemical expression of activated caspase-3 in human myocardial infarction. Virchows Archiv 2006 448 75-79. 

Schwarz K, Simonis G, Yu X, Wiedemann S, Strasser RH. Apoptosis at a distance Remote activation of caspase-3 occurs early after myocardial infarction. Mol Cell Biochem 2006 281 45-54. 

Yarbrough WM, Mukherjee R, Escobar GP, Sample JA, McLean JE, Dowdy KB, et al. Pharmacologic inhibition of intracellular caspases after myocardial infarction attenuates left ventricular remodeling A potentially novel pathway. J Thorac Cardiovasc Surg 2003 126 1892-1899. 

Chandrashekhar Y, Sen S, Anway R, Shuros A, Anand I. Long-term caspase inhibition ameliorates apoptosis, reduces myocardial troponin-1 cleavage, protects left ventricular function, and attenuates remodeling in rats with myocardial infarction. J Am Coll Cardiol 2004 43 295-301. 

Huang JQ, Radinovic S, Rezaiefar P, Black SC. In vivo myocardial infarct size reduction by a caspase inhibitor administered after the onset of ischemia. Eur J Pharmacol 2000 402 139-142. 

Mocanu MM, Baxter GF, Yellon DM. Caspase inhibition and limitation of myocardial infarct size Protection against lethal reperfusion injury. Br J Pharmacol 2000 130 197-200. 

Okamura T, Miura T, Takemura G, Fujiwara H, Iwamoto H, Kawamura S, et al. Effect of caspase inhibitors on myocardial infarct size and myocyte DNA fragmentation in the ischemia-reperfused rat heart. Cardiovasc Res 2000 45 642-650. 

The family of cysteine proteases, which are called caspases, plays a major role in the execution of apoptotic cell death (12). Many studies suggest that increased apoptosis and caspase activity contribute to tissue damage in both acute (e.g., myocardial infarction, stroke, sepsis, spinal cord injury) and chronic (e.g., Alzheimer s, Parkinson s, Huntington s disease) human diseases (13,14). Caspase family members are also prominently... 

Kreuter M, et al. Stroke, myocardial infarction, acute and chronic inflammatory diseases caspases and other apoptotic molecules as targets for drug development. Arch. Immunol. Ther. Exp. 

Balsam LB, Kofidis T, Robbins RC. Caspase-3 inhibition preserves myocardial geometry and long-term function after infarction. J Surg Res 2005 124 194-200. 

CORM-3 protected cardiac cells against hypoxia and reperfusion, as well as limited infarct size in hearts following ischemic insult [32]. In a mice model of heart ischemia and reperfusion (coronary occlusion/reperfusion), CORM-3 promoted similar cardioprotective effects, via decreasing the apoptotic markers, such as cleaved lamin, cleaved caspase-3, and cleaved PARP-1 [77]. CORM-2 also presented cardioprotective effects against myocardial ischemia-reperfusion [78] and doxorubicin-induced cardiotoxicity, which has been a drug used in human malignancies for decades [79]. 

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