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Last update 08 May 2025

Kashin-Beck Disease

Last update 08 May 2025

Basic Info

Synonyms

Disease, Kashin-Beck, Endemic polyarthritis, Kaschin-Beck

+ [21]

Introduction

Disabling osteochondrodysplasia with OSTEOSCLEROSIS, cone-shaped METAPHYSIS, and shortening of the DIAPHYSIS. It is endemic in parts of Siberia and northern China. Mineral deficiencies (e.g., selenium, iodine), fungal cereal contamination, and water contamination may be contributing factors in its etiology.

Drugs associated with Kashin-Beck Disease

TengHuangJianGu

Target-

Mechanism-

Active Org.

Hunan Fangsheng Pharmaceutical Co., Ltd.

Originator Org.

Hunan Fangsheng Pharmaceutical Co., Ltd.

Active Indication

Hyperostosis [+3]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

China

First Approval Date31 Mar 2009

Clinical Trials associated with Kashin-Beck Disease

ChiCTR2400092488

/ SuspendedPhase 4IIT

A randomized controlled trial of aspirin or rivaroxaban for the prevention of venous thromboembolism after primary total hip and total knee arthroplasty

Start Date20 Nov 2024

Sponsor / Collaborator-

ChiCTR2400090636

/ SuspendedNot ApplicableIIT

Analysis of the pH value of synovial fluid in different joint diseases

Start Date14 Oct 2024

Sponsor / Collaborator-

ChiCTR2400090655

/ SuspendedNot ApplicableIIT

Effects of perioperative procedures on skin microbial composition in patients undergoing hip or knee surgery

Start Date14 Oct 2024

Sponsor / Collaborator-

100 Clinical Results associated with Kashin-Beck Disease

100 Translational Medicine associated with Kashin-Beck Disease

0 Patents (Medical) associated with Kashin-Beck Disease

602

Literatures (Medical) associated with Kashin-Beck Disease

01 Jun 2025·Molecular Immunology

LncRNA XIST inhibits mitophagy and increases mitochondrial dysfunction by promoting BNIP3 promoter methylation to facilitate the progression of KBD

Article

Author: Liu, Ruoxi ; Lin, Zhaoxing ; Xiao, Yi ; Zeng, Sixiang ; Dong, Jun ; Wang, Mengxin ; Wu, Wei ; Song, Huanjin ; Huang, Sihua ; Li, Yongwei ; Wu, Hao ; Zhang, Sanpeng ; Ye, Jintao

The primary mechanisms underlying cartilage destruction in Kashin-Beck disease (KBD) involve excessive chondrocyte death and extracellular matrix (ECM) degradation. While long non-coding RNA XIST (lncRNA XIST) has been implicated in promoting chondrocyte injury in osteoarthritis (OA), its role in KBD-related chondrocyte injury remains poorly understood. In this study, joint tissues were collected from four healthy and four KBD-affected children, as well as five healthy and five KBD-affected adults, to assess the expression of lncRNA XIST. The results revealed a significant upregulation of lncRNA XIST in the cartilage tissues of KBD patients. To model KBD-induced chondrocyte damage in vitro, hypertrophic ATDC5 cells were exposed to 10 ng/ml T-2 toxin for 24 hours, which resulted in increased lncRNA XIST expression. Silencing lncRNA XIST was found to mitigate T-2 toxin-induced ECM degradation and chondrocyte apoptosis by alleviating defects in mitochondrial autophagy and dysfunction. Mechanistically, lncRNA XIST promoted the methylation of the BNIP3 promoter by recruiting DNA methyltransferases (DNMTs) to the BNIP3 promoter region, thereby suppressing BNIP3-mediated mitophagy and exacerbating mitochondrial dysfunction. To establish a KBD rat model, rats were fed a low-selenium diet supplemented with T-2 toxin for four weeks. Knockdown of lncRNA XIST in these rats attenuated articular cartilage damage and apoptosis, while enhancing collagen II expression. In conclusion, lncRNA XIST accelerates KBD progression by inhibiting mitophagy and promoting mitochondrial dysfunction through increased BNIP3 promoter methylation.

01 Apr 2025·Journal of Biochemical and Molecular Toxicology

Investigating the Role and Regulatory Mechanisms of the Histone Deacetylase 4 Gene in Chondrocyte Differentiation Impairments Associated With Kashin–Beck Disease

Article

Author: Zhou, Jie ; Yang, Lei ; Wang, Chaowei ; Liu, Lian ; Wang, Xi ; Chen, Feihong ; Bai, Lulu ; Guo, Xiong ; Yi, Shuangqiang

ABSTRACTThis study aimed to investigate the role of the HDAC4 gene in the pathogenesis of Kashin–Beck disease (KBD) cartilage injury and chondrocyte differentiation induced by T‐2 toxin. Immunohistochemistry was used to compare HDAC4 and PTHrP protein expression levels in cartilage from children and adults who have KBD and from respective controls, as well as in cartilage from a rat model exposed to T‐2 toxin and selenium deficiency. A KBD cell model was established by exposure to T‐2 toxin, and RNA interference was employed to silence HDAC4. Expression levels of mRNA and protein expression levels were subsequently measured before and after HDAC4 gene silencing for genes related to the PTHrP–HDAC4 signaling pathway and cartilage differentiation by real‐time quantitative reverse transcription PCR and western blotting. We found that HDAC4 expression levels were not consistent between adult and child chondrocytes. Silencing of HDAC4 resulted in a significant increase in the mRNA expression of Runx2 and PTHrP, and elevated the levels of both the mRNA and protein of MMP13, and increased both the mRNA and protein levels of MEF2C. Notably, following the addition of T‐2 toxin, there was a significant increase in Runx2 expression, whereas the levels of MEF2C and MMP13 were markedly decreased in comparison to pre‐silencing conditions. These findings indicate that T‐2 toxin may influence HDAC4 expression, and the role and regulatory mechanisms of this gene in impairing the differentiation of KBD chondrocytes were explored, thereby offering novel insights into the pathogenesis of KBD.

01 Mar 2025·Environmental Pollution

Downregulation of HSP47 triggers ER stress-mediated apoptosis of hypertrophic chondrocytes contributing to T-2 toxin-induced cartilage damage

Article

Author: Zhang, Ying ; Zhang, Meng ; Shi, Yawen ; Chen, Jinghong ; Wang, Hui ; Ma, Tianyou ; Liu, Yinan

T-2 toxin contamination in food and feed is a growing global concern, with its toxic effects on developing cartilage remaining poorly understood. In this study, we constructed an animal model using 4-week-old male Sprague-Dawley rats, which were administered T-2 toxin (200 ng/g body weight per day) by gavage for one month. Histological analysis showed a significant reduction in hypertrophic chondrocytes and increased caspase-3 expression and TUNEL staining in the deep cartilage zone of T-2 toxin-treated rats. T-2 toxin exposure significantly decreased the expression of heat shock protein 47 (HSP47) and elevated ER stress-mediated apoptosis markers (BiP, caspase-12, and CHOP) in the cartilage of T-2 toxin-treated rats. In an in vitro hypertrophic ATDC5 chondrocyte model, T-2 toxin exposure (10, 25, 50 ng/mL) reduced cell viability and HSP47 expression, while increasing the expression of BiP, caspase-12, and CHOP. Treatment with the ER stress inhibitor Salubrinal suppressed the upregulation of caspase-3 activity, BiP, caspase-12, and CHOP while partially restoring HSP47 expression in T-2 toxin-treated hypertrophic ATDC5 chondrocytes. Furthermore, Hsp47 knockdown in hypertrophic ATDC5 chondrocytes increased the apoptosis ratio, caspase-3 activity, and the expression of BiP, caspase-12, and CHOP. In children with Kashin-Beck disease, a human condition associated with T-2 toxin exposure, reduced HSP47 expression and increased BiP and CHOP expression were observed in the deep zone of articular cartilage. These findings demonstrated that T-2 toxin-induced cartilage damage primarily involves hypertrophic chondrocyte apoptosis in the deep zone. Downregulation of HSP47 leads to ER stress-mediated apoptosis in T-2 toxin-induced cartilage damage. Inhibition of ER stress offers a potential therapeutic approach for mitigating T-2 toxin-induced cartilage damage.

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Kashin-Beck Disease

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