Original ArticleAnthracycline-induced Tension in Permeabilized Cardiac Fibers: Evidence for the Activation of the Calcium Release Channel of Sarcoplasmic Reticulum
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Protective effects of curcumin against doxorubicin-induced toxicity and resistance: A review
2018, Critical Reviews in Oncology/HematologyCitation Excerpt :Intracellular Ca++ overload in the ventricle and mitochondria induced by DOX carries a lowering impact on an expenditure of energy, ending up as the depletion of high-energy phosphates (Ohhara et al., 1981). Besides this, DOX can cause changes in the transport and release of Ca++ in the myocardium (Boucek et al., 1993; Dodd et al., 1993; Ondrias et al., 1990). However, there has been conflicting evidence that cardiomyopathy due to DOX therapy initially relies more on Ca++ depletion rather than its accumulation (Zhou et al., 2001b).
Cellular and Molecular Perspectives on Cardiac Toxins
2015, Heart and ToxinsAliskiren attenuates myocardial apoptosis and oxidative stress in chronic murine model of cardiomyopathy
2012, Biomedicine and PharmacotherapyCitation Excerpt :Oxidative stress. Serum CK-MB and LDH are important myocardial enzymes in the evaluation of myocardial injury and congestive heart failure [47]. The serum levels of these enzymes were significantly elevated in the DXR treated group, whereas higher doses of ALK prevented this increase, indicating that direct inhibition of renin has cardioprotective efficacy against DXR toxicity.
Toxicokinetics of the active doxorubicin metabolite, doxorubicinol, in sulphur-crested cockatoos (Cacatua galerita)
2007, Research in Veterinary ScienceProtective Effects of Carvedilol Against Anthracycline-Induced Cardiomyopathy
2006, Journal of the American College of CardiologyCitation Excerpt :Doxorubicin causes down-regulation of SERCA2 messenger RNA in animals with cardiac dysfunction (21). In addition, ANT has been noted to stimulate the release of Ca2+in cardiomyocytes (22). Carvedilol restores SERCA2 promoter activity in myocytes and it can block down-regulation of SERCA2 gene expression independent of its beta-blocking activity (23).