Cardiovascular disease is the leading cause of death among both women and men, but there is still a great percentage of misdiagnosis and lack of clearly defined criteria. Advances in biomolecular science have proven the crucial role of inflammation and, more importantly, the role of adipokines in mediating all stages of coronary artery disease. It has also been suggested that regional fat deposits, more precisely from thoracic region, have a major influence on the development of coronary artery disease by creating a local proatherogenic environment. The immune system closely interacts with metabolic risk factors to initiate, promote, and further aggravate the atherosclerotic lesions on the arterial wall all with the “help” of adipokines. So nowadays, research extensively focuses on uncovering biomarkers that would provide an increased chance of detecting subclinical cardiac distress and also add a consistent value to current guideline-imposed risk criteria.

Drug-induced cardiotoxicity is a life-threatening side effect of doxorubicin (DOX) treatment that impacts patient prognosis and survival. In the majority of cases, the acute clinical form often remains asymptomatic, with few patients presenting rather nonspecific electrocardiographic abnormalities. While chronic toxicity has been more widely studied, the alterations appearing in acute cardiotoxicity are much less investigated. Thus, our in vivo study aimed to evaluate the process of DOX-induced acute myocardial toxicity by investigating oxidative stress and autophagy markers as mechanisms of myocardial toxicity in correlation with echocardiography and electrocardiography findings. Our results show that both autophagy and oxidative homeostasis were disrupted as soon as 7 days after DOX treatment, alterations that occurred even before the significant increase of NT-proBNP, a clinical marker for cardiac suffering. Moreover, we found a large number of alterations in the electrocardiography and echocardiography of treated rats. These findings suggest that DOX-induced myocardial toxicity started early after treatment initiation, possibly marking the initial phase of the unfolding process of cardiac damage. Further studies are required to completely decipher the mechanisms of DOX-induced cardiotoxicity. Graphical Abstract

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