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细胞损伤的分子机制及毒性重金属在慢性肾脏病中的作用。

Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease.

机构信息

Department of Biomedical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA.

Department of Pathology and Clinical Sciences Education, Mercer University School of Medicine, Macon, GA 31207, USA.

出版信息

Int J Mol Sci. 2022 Sep 21;23(19):11105. doi: 10.3390/ijms231911105.

Abstract

Chronic kidney disease (CKD) is a progressive disease that affects millions of adults every year. Major risk factors include diabetes, hypertension, and obesity, which affect millions of adults worldwide. CKD is characterized by cellular injury followed by permanent loss of functional nephrons. As injured cells die and nephrons become sclerotic, remaining healthy nephrons attempt to compensate by undergoing various structural, molecular, and functional changes. While these changes are designed to maintain appropriate renal function, they may lead to additional cellular injury and progression of disease. As CKD progresses and filtration decreases, the ability to eliminate metabolic wastes and environmental toxicants declines. The inability to eliminate environmental toxicants such as arsenic, cadmium, and mercury may contribute to cellular injury and enhance the progression of CKD. The present review describes major molecular alterations that contribute to the pathogenesis of CKD and the effects of arsenic, cadmium, and mercury on the progression of CKD.

摘要

慢性肾脏病(CKD)是一种进行性疾病,每年影响数以百万计的成年人。主要的危险因素包括糖尿病、高血压和肥胖,这些疾病影响着全球数以百万计的成年人。CKD 的特征是细胞损伤,随后功能性肾单位永久丧失。随着受损细胞死亡和肾单位发生硬化,剩余的健康肾单位通过各种结构、分子和功能变化来试图代偿。虽然这些变化旨在维持适当的肾功能,但它们可能导致额外的细胞损伤和疾病进展。随着 CKD 的进展和滤过率降低,清除代谢废物和环境毒物的能力下降。无法清除环境毒物,如砷、镉和汞,可能导致细胞损伤并加速 CKD 的进展。本综述描述了导致 CKD 发病机制的主要分子改变,以及砷、镉和汞对 CKD 进展的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f942/9569673/8b2750d35b6c/ijms-23-11105-g001.jpg

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