Columbia University Division of Cardiology, Mount Sinai Medical Center, 4300 Alton Road, Suite # 2070A, Miami Beach, FL, 33140, USA.
Department of Medicine, Mount Sinai Medical Center, Miami Beach, FL, USA.
Curr Environ Health Rep. 2021 Mar;8(1):42-53. doi: 10.1007/s40572-021-00304-w. Epub 2021 Mar 23.
Cadmium has been recognized as a potential risk factor for cardiovascular disease (CVD). We present a review of cadmium toxicity, its effect on cellular activities, and a summary of reported association between environmental cadmium exposure and CVD. We also discuss the possible therapeutic benefit of cadmium chelation.
Experimental data suggest that cadmium affects several signaling pathways which may lead to endothelial dysfunction and vascular tissue damage, promoting atherosclerosis. This is further supported by epidemiological studies that have shown an association of even low-level cadmium exposure with an increased risk of clinical cardiovascular events. The Trial to Assess Chelation Therapy (TACT) provided inferential evidence for the cardiovascular benefit of treating toxic metal burden. However, at the present time, there is no direct evidence, but suggestive findings from clinical trials indicating that removal of cadmium from body stores may be associated with improved cardiovascular outcomes. An evolving body of evidence supports environmental cadmium exposure as a pro-atherosclerosis risk factor in CVD; however, the mechanisms for the proatherogenic effect of cadmium are still not completely understood. Further studies in translational toxicology are needed to fill the knowledge gaps regarding the molecular mechanisms of cadmium toxicity and the promotion of atherosclerosis.
镉已被认为是心血管疾病（CVD）的潜在危险因素。我们对镉毒性、其对细胞活动的影响以及环境镉暴露与 CVD 之间的关联进行综述，并讨论了镉螯合的可能治疗益处。
实验数据表明，镉会影响多种信号通路，从而导致内皮功能障碍和血管组织损伤，促进动脉粥样硬化。这一观点得到了流行病学研究的进一步支持，这些研究表明，即使是低水平的镉暴露也会增加临床心血管事件的风险。评估螯合疗法的试验（TACT）提供了关于治疗毒性金属负荷对心血管有益的推论证据。然而，目前没有直接证据，但临床试验的提示性发现表明，从体内储存中去除镉可能与改善心血管结局相关。越来越多的证据支持环境镉暴露是 CVD 中动脉粥样硬化的促发因素；然而，镉的促动脉粥样硬化作用的机制仍不完全清楚。需要在转化毒理学方面开展进一步的研究，以填补关于镉毒性和促进动脉粥样硬化的分子机制的知识空白。
