Mitochondria are central organelles in the homeostasis of the cardiovascular system via the integration of several physiological processes, such as ATP generation via oxidative phosphorylation, synthesis/exchange of metabolites, calcium sequestration, reactive oxygen species (ROS) production/buffering and control of cellular survival/death. Mitochondrial impairment has been widely recognized as a central pathomechanism of almost all cardiovascular diseases, rendering these organelles important therapeutic targets. Mitochondrial dysfunction has been reported to occur in the setting of drug-induced toxicity in several tissues and organs, including the heart. Members of the drug classes currently used in the therapeutics of cardiovascular pathologies have been reported to both support and undermine mitochondrial function. For the latter case, mitochondrial toxicity is the consequence of drug interference (direct or off-target effects) with mitochondrial respiration/energy conversion, DNA replication, ROS production and detoxification, cell death signaling and mitochondrial dynamics. The present narrative review aims to summarize the beneficial and deleterious mitochondrial effects of common cardiovascular medications as described in various experimental models and identify those for which evidence for both types of effects is available in the literature.

Sodium-glucose co-transporter (SGLT) inhibitors are a novel class of glucose-lowering drugs with beneficial pleiotropic effects that have been widely investigated in the past decade in several experimental models and patients in the absence of diabetes. There are two types of transporters: the SGLT1 isoform that is distributed across a broad range of tissues, including the cardiovascular system, and the SGLT2 isoform, which is mostly expressed in renal proximal tubular cells. It is known that inflammation and oxidative stress are key contributors to vascular damage and the progression of atherosclerosis. SGLT inhibitors have demonstrated multiple benefits that contribute to improved vascular health, including alleviation of endothelial function, anti-inflammatory and antioxidative effects, and mitigation of arterial stiffness, all contributing to blood pressure decrease. An increasing body of research has tackled the molecular and cellular mechanisms of their chronic and, more recently, acute cardiovascular beneficial effects. This narrative review specifically delves into the direct vasculoprotective effects of SGLT2 and dual SGLT1/2 inhibitors, summarizing their off-target mechanisms described in various experimental settings (animal models, animal and human cell lines/samples).

Oxidative stress has emerged as an important component of the complex pathophysiology of inflammatory bowel disease (IBD), where increasing evidence suggests an interaction between redox imbalance, immune activation, epithelial dysfunction, and chronic intestinal inflammation. This structured narrative review critically synthesizes current evidence regarding the biological basis of oxidative stress in IBD, with emphasis on cellular and molecular mechanisms, oxidative biomarkers, therapeutic modulation of redox pathways, and their translational relevance. Current evidence indicates that oxidative stress is associated with immune-cell activation, mitochondrial dysfunction, impairment of epithelial homeostasis, and dysregulation of redox-sensitive signaling pathways. Biomarkers including nitric oxide metabolites, malondialdehyde, myeloperoxidase, total antioxidant capacity, serum thiols, and antioxidant enzymes have demonstrated associations with inflammatory activity, while anti-inflammatory, antioxidant, and dietary interventions have been reported to modulate oxidative biomarkers in selected clinical studies. However, substantial methodological heterogeneity, variability in analytical techniques, and limited prospective validation currently restrict their routine clinical application. Moreover, many mechanistic pathways have been characterized predominantly in experimental models, highlighting the need to distinguish biological plausibility from evidence supporting clinical implementation. Overall, oxidative stress represents a promising area of investigation that may contribute to a better understanding of IBD biology and support future biomarker-guided and precision medicine approaches. Nevertheless, further standardized translational and longitudinal clinical studies are required before oxidative biomarkers and redox-targeted strategies can be integrated into routine patient care.