Mecanismos moleculares da cardiotoxicidade induzida por esteroides anabolizantes: integração entre dislipidemia, estresse oxidativo, inflamação e remodelamento cardíaco

Abstract

The non-therapeutic use of anabolic-androgenic steroids (AAS) has increased over recent decades, becoming a significant public health concern, particularly among young adults exposed to supraphysiological doses for aesthetic and performance-enhancing purposes. Although the cardiovascular effects associated with AAS are widely recognized, the underlying pathophysiological mechanisms are still often described in a fragmented manner, hindering a comprehensive understanding of AAS-induced cardiotoxicity. In this context, the present study aimed to analyze the main molecular mechanisms involved in AAS-induced cardiovascular alterations, with emphasis on the interaction among dyslipidemia, oxidative stress, inflammation, and cardiac remodeling. The evidence demonstrated that AAS-related cardiovascular toxicity is multifactorial, involving significant dysregulation of lipid metabolism, mainly characterized by reduced HDL levels and, in some cases, increased LDL levels, resulting in an atherogenic lipid profile. This dyslipidemia is associated with increased production of reactive oxygen species, which activate redox-sensitive inflammatory pathways, intensifying endothelial injury and promoting the progression of atherosclerosis. Furthermore, AAS induce direct structural alterations in the myocardium, including concentric hypertrophy, myocardial fibrosis, diastolic stiffness, and electrical instability, findings suggestive of pathological cardiac remodeling. Therefore, it can be concluded that AAS-induced cardiotoxicity results from the interaction among atherogenic dyslipidemia, oxidative stress, inflammatory activation, and cardiac remodeling, mechanisms that act in an integrated manner to drive the progression of cardiovascular damage.