Why the study?
Doxorubicin has undesirable effects on the heart that lead to cardiac dysfunction, motivating a review of how toxicity disrupts contractile machinery and associated factors.
Doxorubicin induces cardiotoxicity by causing oxidative stress that damages cardiac contractile proteins and calcium-handling mechanisms, leading to left ventricular dysfunction.
May support closer cardiac monitoring with doxorubicin; leaves open whether targeting these pathways alters outcomes.
Doxorubicin (DOX) is a boon for cancer‐suffering patients. However, the undesirable effect on health on vital organs, especially the heart, is a limiting factor, resulting in an increased number of patients with cardiac dysfunction. The present review focuses on the contractile machinery and associated factors, which get affected due to DOX toxicity in chemo‐patients for which they are kept under life‐long investigation for cardiac function. DOX‐induced oxidative stress disrupts the integrity of cardiac contractile muscle proteins that alter the rhythmic mechanism and oxygen consumption rate of the heart. DOX is an oxidant and it is further discussed that oxidative stress prompts the damage of contractile components and associated factors, which include Ca 2+ load through Ca 2+ ATPase, SERCA, ryanodine receptor‐2, phospholamban, and calsequestrin, which ultimately results in left ventricular ejection and dilation. Based on data and evidence, the associated proteins can be considered as clinical markers to develop medications for patients. Even with the advancement of various diagnosing tools and modified drugs to mitigate DOX‐induced cardiotoxicity, the risk could not be surmounted with survivors of cancer.
No takes yet. Share an insight, caveat, or question.
Upadhyay et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: