Subchronic exposure to cigarette smoke has been shown to induce pathological changes in various organ systems, including the cardiovascular system. This literature review synthesizes current evidence on the effects of subchronic cigarette smoke exposure on mouse cardiomyocytes, with a focus on oxidative stress, mitochondrial dysfunction, genetic regulation, contractile function, and inflammation. Experimental models typically involve whole-body or nose-only exposure for several weeks, simulating human subchronic exposure patterns. Mechanistic findings reveal increased reactive oxygen species (ROS) production, impaired mitochondrial respiration, and disruption of antioxidant defense systems, particularly involving superoxide dismutase (SOD) and adenine nucleotide translocator (ANT). Gene expression studies demonstrate altered regulation of apoptotic, inflammatory, and metabolic pathways, accompanied by epigenetic modifications such as DNA methylation and microRNA dysregulation. Functional assessments indicate decreased cardiomyocyte viability, reduced contractile activity, and increased cellular senescence. Inflammatory responses are characterized by elevated cytokine production, including TNF-α and IL-6, which may contribute to myocardial remodeling. While evidence strongly suggests a detrimental effect of subchronic cigarette smoke on mouse cardiomyocytes, limitations remain due to the scarcity of long-term follow-up studies and direct translational models in humans. Future research should focus on targeted interventions to mitigate oxidative and inflammatory damage in cardiomyocytes exposed to tobacco smoke.
Ratsmawan et al. (Fri,) studied this question.