Diabetic cardiomyopathy

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Ganguly P.K., Pierce G.N., Dhalla K.S., Dhalla N.S. Defective sarcoplasmic reticular calcium transport in diabetic cardiomyopathy. Am. J. Physiol. 244 (1983) E528-E535. 

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Tappia P.S., Asemu G., Aroutiounova N., Dhalla N.S. Defective sarcolemmal phospholipase C signaling in diabetic cardiomyopathy. Mol. Cell. Biochem. 261 (2004a) 193-199. 

Gqa/PLCPi signahng in diabetic cardiomyopathy. J. Mol. Cell. Cardiol. 32 (2000) A46. 

Tappia P.S., Maddaford T.G., Hurtado C., Dibrov E., Austria J.A., Sahi N., Panagia V., Pierce G.N. Defective phosphatidic acid-phosphohpase C signaling in diabetic cardiomyopathy. Biochem. Biophys. Res. Commun. 316 (2004b) 280-289. 

Tong Y., Liu S-Y., Tappia P.S., Panagia V. Sarcolemmal PLC yj is hypoactive but hyperre-sponsive to phosphatidic acid in diabetic cardiomyopathy (Abstract). J. Mol. Cell. Cardiol. 30 (1998) A257. 

Isfort, M Stevens, SCW Schaffer, S Jong, CJ Wold, LE. Metabolic dysfunction in diabetic cardiomyopathy. Heart Fail Rev, 2014 19 35-48. 

Kohda, Y., Shirakawa, H., Yamane, K., Otsuka, K., Kono, T., Terasaki, F., and Tanaka, T., 2008. Prevention of incipient diabetic cardiomyopathy by high-dose thiamine. The Journal of Toxicological Sciences. 33 459 72. 

This condition is referred to as ischemia-reperfusion injury. Several studies in animal models of ischemia-reperfusion injury have shown that the principal cause of cellular death is necrosis (11-13). However, other smdies have shown that cellular death consisted of a necrotic core surrounded by a peri-necrotic area that displayed properties consistent with apoptosis (11,14-18). Therefore, it is likely that cellular death resulting from ischemia-reperfusion injury can consist of a mixture of apoptosis and necrosis, depending on the extent and duration of the ischemia prior to reperfusion. Other disease conditions where evidence demonstrating both apoptosis and necrosis occur includes diabetic cardiomyopathy, sepsis, stroke, and the neurodegenerative disorders Alzheimer s disease and Parkinson s disease. The development of a noninvasive imaging technique capable of measuring apoptosis and necrosis independently could provide valuable information on the balance between apoptosis and necrosis, and if there is a temporal shift in the balance of these mechanisms of cellular death, in a wide variety of pathological conditions. 

As stated earlier, the overactivation of PARP-1 levels and depletion of NAD" " pools is currently believed to be the principal pathway responsible for cellular death via necrosis. Therefore, PARP-1 is thought to play a major role in a variety of pathological conditions including ischemia—reperfiision injury (i.e., myocardial infarction and stroke), septic shock, diabetic cardiomyopathy, and neurodegeneration (Table 13.2). The measurement of PARP-1 levels is currently limited to the use of immunohistochemistry techniques in tissue slices. The development of a radiotracer that could image PARP-1 levels with PET and SPECT would provide a useful tool in smdying the role of this enzyme in a variety of pathological conditions. 

Total triterpenic acids isolated from Cornus officinalis fruits ameliorate diabetic cardiomyopathy in streptozocin-injected rats, by suppressing the endothelin reactive oxidative species pathway in the myocardium [Qi et al., 2008]. 

Yoon, Y. S., Uchida, S., Masuo, O., Cejna, M., Park, J. S., Gwon, H. C., Kirchmair, R., Bahlman, E, Walter, D., Curry, C., Hanley, A., Isner, J. M., and Losordo, D. W. 2005. Progressive attenuation of myocardial vascular endothelial growth factor expression is a seminal event in diabetic cardiomyopathy—Restoration of microvascular homeostasis and recovery of cardiac function in diabetic cardiomyopathy after replenishment of local vascular endothehal growth factor. Circulation, 111, 2073-2085. 

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