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

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  FIGURE 1. Cur‐mediated modulation of SOD‐centered redox and signalling networks in CVD. Curcumin (Cur) exerts cardioprotective effects through coordinated regulation of multiple interconnected signalling pathways that converge on superoxide dismutase (SOD) isoforms (SOD1, SOD2 and SOD3), which serve as a central hub of redox homeostasis. Cur activates antioxidant pathways via nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant response element (ARE) signalling, leading to increased expression of SOD and downstream cytoprotective enzymes, including heme oxygenase‐1 (HO‐1) and NAD(P)H quinone dehydrogenase 1 (NQO1). Concurrently, Cur suppresses inflammatory signalling by inhibiting nuclear factor‐kappa B (NF‐κB) and reducing pro‐inflammatory mediators, such as tumour necrosis factor‐α (TNF‐α), interleukin (IL)‐1β and inducible nitric oxide synthase (iNOS). Cur further modulates cell survival and metabolic pathways through activation of phosphatidylinositol‐3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), Sirtuin 1 (SIRT1) and AMP‐activated protein kinase (AMPK). In parallel, Cur attenuates stress‐induced cell death mechanisms, including ferroptosis,…

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  FIGURE 2. Disease‐oriented summary of curcumin‐mediated modulation of superoxide dismutase (SOD) and cardiovascular outcomes based on in vivo studies (Table 1). This schematic summarizes the disease‐specific effects of curcumin (Cur) on superoxide dismutase (SOD) across major cardiovascular disease (CVD) models derived from in vivo studies presented in Table 1. Curcumin administration consistently enhances SOD activity and/or expression, including cytosolic SOD1, mitochondrial SOD2 and extracellular SOD3, across diverse pathological conditions such as myocardial infarction (MI), cardiomyopathy, hypertension, cardiac toxicity, abdominal aortic aneurysm (AAA) and diabetes mellitus (DM). Upregulation of SOD is associated with attenuation of oxidative stress, as evidenced by reduced malondialdehyde (MDA) levels and decreased reactive oxygen species (ROS) accumulation, along with suppression of inflammatory signalling pathways and improved antioxidant defence systems. These redox improvements translate into reduced apoptosis, fibrosis and extracellular matrix remodelling, as well as improved mitochondrial function and vascular integrity. Consequently, curcumin‐mediated SOD activation…