Mercury-Mediated Cardiovascular Toxicity: Mechanisms and Remedies Publisher Pubmed



Amin A¹ ; Saadatakhtar M² ; Mohajerian A³ ; Marashi SM⁴ ; Zamanifard S⁵ ; Keshavarzian A⁶ ; Molaee P⁴ ; Keshmiri MS⁷ ; Nikdoust F⁸ Show Affiliations
Source: Cardiovascular Toxicology Published:2025

Abstract

Abstract: Mercury is a significant environmental pollutant and public health threat, primarily recognized for its neurotoxic effects. Increasing evidence also highlights its harmful impact on the cardiovascular system, particularly in adults. Exposure to mercury through contaminated soil, air, or water initiates a cascade of pathological events that lead to organ damage, including platelet activation, oxidative stress, enhanced inflammation, and direct injury to critical cells such as cardiomyocytes and endothelial cells. Endothelial activation triggers the upregulation of adhesion molecules, promoting the recruitment of leukocytes and platelets to vascular sites. These interactions activate both platelets and immune cells, creating a pro-inflammatory, prothrombotic environment. A key outcome is the formation of platelet-leukocyte aggregates (PLAs), which exacerbate thromboinflammation and endothelial dysfunction. These processes significantly elevate cardiovascular risks, including thrombosis and vascular inflammation. This study offers a comprehensive analysis of the mechanisms underlying mercury-induced cardiotoxicity, focusing on oxidative stress, inflammation, and cellular dysfunction. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.