Superoxide Dismutase–Centered Modulation by Curcumin in Cardiovascular Diseases: Mechanistic Insights and Translational Implications Publisher Pubmed



Khayatan D ; Razavi S M ; Arab Z N ; Niknejad A ; Hosseini Y ; Kashani A S ; Momtaz S ; Jamialahmadi T ; Kesharwani P ; Abdolghaffari A H ; Sahebkar A
Source: Journal of Cellular and Molecular Medicine Published:2026

Abstract

Cardiovascular diseases (CVD) remain the leading global cause of morbidity and mortality, driven in part by dysregulated redox homeostasis and chronic inflammation. Superoxide dismutase (SOD), a key enzymatic defence against reactive oxygen species (ROS), plays a central role in maintaining cardiovascular integrity through regulation of oxidative stress across cytosolic (SOD1), mitochondrial (SOD2) and extracellular (SOD3) compartments. Impairment of SOD function contributes directly to endothelial dysfunction, myocardial injury and vascular remodelling. Curcumin (Cur), a pleiotropic polyphenol derived from Curcuma longa, has emerged as a potent modulator of SOD activity and expression. Evidence from preclinical models consistently demonstrates that Cur enhances SOD-dependent antioxidant defences, thereby attenuating oxidative damage, inflammation, apoptosis and fibrosis across multiple CVD contexts, including myocardial infarction, cardiomyopathy, hypertension and diabetic complications. While Cur also influences additional signalling pathways, such as NF-κB, PI3K/AKT and Nrf2, these effects are increasingly understood to converge on SOD-mediated redox regulation. Recent advances in nanodelivery systems have further improved Cur bioavailability and its capacity to modulate SOD activity in vivo. However, despite robust preclinical evidence, clinical validation remains limited. This review synthesizes current mechanistic and translational evidence, positioning SOD as the central mediator of Cur's cardioprotective effects and highlights key gaps in clinical translation. © 2026 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.