Sule Rasheed O, Rivera Gabriela Del Toro, Vaidya Tanishq, Gartrell Emily, Gomes Aldrin V
Department of Neurobiology, Physiology, and Behavior, University of California, Davis, CA 95616, USA.
Center for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
Antioxidants (Basel). 2025 May 17;14(5):604. doi: 10.3390/antiox14050604.
Cardiovascular diseases (CVDs) remain a leading global health concern, responsible for substantial morbidity and mortality. In recent years, as our understanding of the multifaceted nature of CVDs has increased, it has become increasingly evident that traditional risk factors alone do not account for the entirety of cardiovascular morbidity and mortality. Environmental toxins, a heterogeneous group of substances ubiquitous in our surroundings, have now entered the spotlight as offenders in the development and progression of CVDs. Environmental toxins include heavy metals, air pollutants, pesticides, and endocrine-disrupting chemicals, among others. Upon exposure, they can elicit oxidative stress, a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify and repair the resulting damage. Oxidative stress triggers a cascade of events, including inflammation, endothelial dysfunction, lipid peroxidation, and vascular remodeling, which can contribute to the development of atherosclerosis, hypertension, and other cardiovascular pathologies. This article delves into the molecular mechanisms underpinning oxidative stress-mediated cardiovascular damage induced by environmental toxins, emphasizing the role of specific toxins in this process. Further research is necessary to understand how individual susceptibility and genotype influence the impact of environmental toxins on oxidative stress and the risk of CVD.
心血管疾病(CVDs)仍然是全球主要的健康问题,导致大量发病和死亡。近年来,随着我们对心血管疾病多方面性质的认识不断加深,越来越明显的是,仅传统危险因素并不能解释心血管疾病发病和死亡的全部情况。环境毒素是我们周围普遍存在的一类异质性物质,现已成为心血管疾病发生和发展的罪魁祸首而备受关注。环境毒素包括重金属、空气污染物、农药以及内分泌干扰化学物质等。接触这些毒素后,它们会引发氧化应激,其特征是活性氧(ROS)生成与身体解毒和修复由此产生损伤的能力之间失衡。氧化应激引发一系列事件,包括炎症、内皮功能障碍、脂质过氧化和血管重塑,这些都可能导致动脉粥样硬化、高血压和其他心血管疾病的发生。本文深入探讨环境毒素诱导氧化应激介导心血管损伤的分子机制,强调特定毒素在此过程中的作用。有必要进行进一步研究,以了解个体易感性和基因型如何影响环境毒素对氧化应激和心血管疾病风险的影响。