Zinc: a metallic shield against cardiac inflammation.

Abstract

Zinc (Zn) is a trace element essential for the function of over 10% of the human proteome, yet the average adult body contains only about two grams. Despite its trace status, Zn plays an indispensable role in immune regulation, inflammation control, and redox signalling. Low Zn status is associated with impaired immune function and increased oxidative stress-factors that critically contribute to the pathogenesis of cardiac inflammatory diseases (CIDs), including myocarditis and pericarditis. These conditions are rising in incidence globally, particularly in younger adults, and are linked to viral infections, autoimmune triggers, and post-vaccination inflammatory responses. Zn not only protects cysteine thiol groups from oxidation but also acts as a redox-sensitive secondary messenger via the "Redox Zinc Switch" mechanism-a key process in modulating cellular responses to oxidative stress. In the cardiovascular system, Zn influences antioxidant defence, cytokine regulation, and membrane repair pathways, including cellular responses that are regulated by protein kinase C and metallothioneins. Emerging evidence supports Zn supplementation as a strategy to mitigate myocardial inflammation, reduce cardiac remodelling, and improve outcomes in oxidative stress driven heart diseases. This review synthesizes current knowledge on Zn's biochemical, immunological, and therapeutic roles in cardiac inflammation. We argue that maintaining optimal Zn levels through diet or supplementation represents a promising, accessible intervention to reduce the burden of CIDs and improve cardiovascular resilience in at-risk populations.