College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu 225009, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu 225009, PR China; Joint International Research Laboratory of Agriculture and Agri-Product Safety of the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu 225009, PR China.
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu 225009, PR China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu 225009, PR China; Joint International Research Laboratory of Agriculture and Agri-Product Safety of the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu 225009, PR China.
Sci Total Environ. 2021 May 15;769:144646. doi: 10.1016/j.scitotenv.2020.144646. Epub 2021 Jan 18.
Cadmium (Cd) is a widespread environmental contaminant that causes severe bone metabolism disease, such as osteoporosis, osteoarthritis, and osteomalacia. The present review aimed to explore the molecular mechanisms of Cd-induced bone injury starting from bone cell function and teeth development. Cd inhibits the differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts, and directly causes BMSC apoptosis. In the case of osteoporosis, Cd mainly affects the activation of osteoclasts and promotes bone resorption. Cd-induces osteoblast injury and oxidative stress, which causes DNA damage, mitochondrial dysfunction, and endoplasmic reticulum stress, resulting in apoptosis. In addition, the development of osteoarthritis (OA) might be related to Cd-induced chondrocyte damage. The high expression of metallothionein (MT) might reduce Cd toxicity toward osteocytes. The toxicity of Cd toward teeth mainly focuses on enamel development and dental caries. Understanding the effect of Cd on bone cell function and teeth development could contribute to revealing the mechanisms of Cd-induced bone damage. This review explores Cd-induced bone disease from cellular and molecular levels, and provides new directions for removing this heavy metal from the environment.
镉(Cd)是一种广泛存在的环境污染物,可导致严重的骨骼代谢疾病,如骨质疏松症、骨关节炎和佝偻病。本综述旨在从骨细胞功能和牙齿发育两方面探讨 Cd 诱导的骨骼损伤的分子机制。Cd 抑制骨髓间充质干细胞(BMSCs)向成骨细胞的分化,并直接导致 BMSC 凋亡。在骨质疏松症的情况下,Cd 主要影响破骨细胞的激活并促进骨吸收。Cd 诱导成骨细胞损伤和氧化应激,导致 DNA 损伤、线粒体功能障碍和内质网应激,从而引发细胞凋亡。此外,骨关节炎(OA)的发展可能与 Cd 诱导的软骨细胞损伤有关。金属硫蛋白(MT)的高表达可能会降低 Cd 对成骨细胞的毒性。Cd 对牙齿的毒性主要集中在釉质发育和龋齿上。了解 Cd 对骨细胞功能和牙齿发育的影响有助于揭示 Cd 诱导骨骼损伤的机制。本综述从细胞和分子水平探讨了 Cd 诱导的骨骼疾病,并为从环境中去除这种重金属提供了新的方向。