Progress and perspectives in exploring the biological mechanisms of early chondrocyte damage in Kashin-Beck disease based on iPSC-derived disease model
10.3760/cma.j.cn231583-20241202-00407
- VernacularTitle:基于iPSCs疾病细胞模型探索大骨节病软骨细胞早期损伤的生物学机制进展与展望
- Author:
Xiong GUO
1
;
Huan LIU
1
Author Information
1. 西安交通大学医学部公共卫生学院地方病研究所 国家卫健委环境与地方性疾病重点实验室 陕西省丝路区域地方病与健康促进协同创新中心，西安 710061
- Publication Type:Journal Article
- Keywords:
Kashin-Beck disease;
Induced pluripotent stem cells;
Mycotoxins;
Disease model
- From:
Chinese Journal of Endemiology
2025;44(10):775-779
- CountryChina
- Language:Chinese
-
Abstract:
To address the key issues of unclear cartilage damage mechanisms, lack of disease models, and targeted interventions in Kashin-Beck disease (KBD), which poses a serious threat to the health of the Chinese population, this article reviews the progress and application of constructing disease cell models that are highly homogeneous with KBD primary chondrocytes both domestically and internationally, providing new scientific basis for further study on the cartilage damage mechanisms of this disease. Firstly, China has successfully constructed an induced pluripotent stem cell (iPSC)-derived disease model that is highly homogeneous with KBD primary chondrocytes, providing stable disease cell resources for in-depth study on the mechanism of cartilage damage in this disease. Based on the KBD-iPSCs-derived disease model, it is found that T-2 toxin, HT-2 toxin, deoxynivalenol (DON), and/or low selenium have an early damaging effect on the KBD-iPSCs disease model. Among them, the combined environmental factors have a more significant effect on KBD-iPSCs chondrocytes damage than a single environmental factor. It is found that selenomethionine (Se-Met) and C-Jun N-terminal kinase 1 (JNK1) inhibitors have protective effects against early damage to KBD-iPSCs chondrocytes. In the future, the KBD-iPSCs-derived disease model can be further applied, combined with the establishment of animal models similar to human cartilage growth and development, to determine the molecular biological mechanisms, biomarkers in early disease stage, and targeted therapies of KBD chondrocytes damage, so as to provide scientific basis for advancing the study on new strategies to eliminate KBD.
