Doxorubicin is really a potent chemotherapeutic agent used for a wide number of malignancies. Because of the rapid disappearance of the sensitive cells in countries, low passage cells were stably transfected with hTERT to reduce mobile senescence, and then subcloned to identify sets of tolerant and sensitive clones. TERT expression could easily alter mRNA expression patterns, and yet, a lot of transcripts and proteins analyzed maintained similar expression in the main and TERT clones. Microarray profiling of the painful and sensitive and resistant clones is underway to recognize further changes related to resistance, and the way the TERT expression alters gene expression. Further studies may also be using siRNA, and forced overexpression, to find out which, if any, of these specialists have a role in the resistance to apoptosis MAPK activation of these lesion cells. However, the current studies have revealed a potential pathway of resistance involving STATs, cyclin D1, BAD, Bcl XL and caspase 1 which may modulate the sensitivity to apoptosis in human lesion cells. This has significant implications for understanding the processes of plaque progression relative to plaque instability and rupture, and may help to design therapeutic strategies to prevent the effect of vascular disease. But, the usage of doxorubicin is limited because of its collective dose dependent cardiotoxicity, which sometimes leads to doxorubicin cardiomyopathy. Oxidative Plastid stress is suggested as one of many mechanisms of cardiotoxicity by doxorubicin, although the exact mechanism of doxorubicin induced cardiotoxicity is not completely understood. Acute or chronic doxorubicin cardiotoxicity is paid off in transgenic mice overexpressing mitochondrial MnSOD or cysteine rich metallothioneins, respectively, supporting the theory that oxidative stress mediates doxorubicin cardiotoxicity. It’s already been suggested a tumor suppressor protein p53 is a crucial mediator of doxorubicin cardiotoxicity. This notion is supported by the observation that doxorubicin causes p53 accumulation in-the center and that either pharmacological or genetic ablation of p53 results in the attenuation of cardiotoxicity following doxorubicin therapy. But, how p53 is activated within the center by doxorubicin or how p53 mediates the cardiotoxic effects Fostamatinib clinical trial of doxorubicin remains elusive. This does not directly demonstrate the role of cardiomyocyte apoptosis in doxorubicin mediated cardiotoxicity, although myocyte apoptosis induced by doxorubicin was attenuated by p53 ablation. It was recently found that p53 stops hypoxia inducible factor 1 and therefore encourages myocardial ischemia. Recently, p53 dependent inhibition of mammalian target of rapamycin was proposed as a process of acute doxorubicin cardiotoxicity independently of p53 induced apoptosis.