查看文章

Animal studies have shown that exposure to tobacco smoke (ETS) leads to inflammation and cardiac remodeling, characterized by heart hypertrophy, higher diastolic dimension of the left ventricle and impaired systolic function [1–3]. Although the precise mechanisms of smoking-induced alterations remain unclear, the evidence supports the hypothesis that oxidative stress and inflammation provide the pathophysiological link between ETS and heart alterations [4, 5]. In recent years, vitamin D has emerged as an important nutrient for heart health and its deficiency has been linked to increased cardiovascular disease risk [6, 7]. In heart aggression models, vitamin D (VD) supplementation attenuated the cardiac remodeling by influencing the contractility, hypertrophy, renin angiotensin system, fibrosis and inflammation [8–10]. Given that vitamin D may modulate cardiac alterations following different injuries, the objective …