Pathways related to mitochondrial dysfunction in cartilage of endemic osteoarthritis patients in China

Chunyan Li,Youfen Li,Weijuan Ma,Weizhuo Wang,Feng Zhang,Yidong Bai,J Mikko Lammi,Yingang Zhang,Xiong Guo

doi:10.1007/s11427-012-4418-4

Abstract

In this paper, we present the first evidence of differences in the mitochondria-related gene expression profiles of adult articular cartilage derived from patients with Kashin-Beck disease and normal controls. The expression of 705 mitochondria-related genes was analyzed by mitochondria-related gene expression analysis and ingenuity pathways analysis. Mitochondria-related gene expression analysis identified 9 up-regulated genes in Kashin-Beck disease based on their average expression ratio. Three canonical pathways involved in oxidative phosphorylation, apoptosis signaling and pyruvate metabolism were identified, which indicate the involvement of mitochondrial dysfunction in the pathogenesis of Kashin-Beck disease.

Highlights

LI ChunYan1,2, WANG WeiZhuo3, GUO Xiong1*, ZHANG Feng1, MA WeiJuan1, ZHANG YinGang4, LI YouFen5, BAI YiDong6 & LAMMI Mikko J7
Three canonical pathways involved in oxidative phosphorylation, apoptosis signaling and pyruvate metabolism were identified, which indicate the involvement of mitochondrial dysfunction in the pathogenesis of Kashin-Beck disease
The findings showed that abnormal mitochondrial function and cell death were involved in the pathophysiology of this disease [6,7], suggesting that mitochondrial dysfunction and apoptosis play important roles in the pathogenesis of Kashin-Beck disease (KBD)

Summary

Introduction

Three canonical pathways involved in oxidative phosphorylation, apoptosis signaling and pyruvate metabolism were identified, which indicate the involvement of mitochondrial dysfunction in the pathogenesis of Kashin-Beck disease. Kashin-Beck disease (KBD) is a chronic, endemic deforming osteoarthrosis, characterized by chondrocyte necrosis and apoptosis, cartilage degeneration and matrix degradation [1]. Various environmental etiologic hypotheses have been proposed, such as selenium deficiency, serious cereal contamination by mycotoxin-producing fungi, and high humic acid levels in drinking water [5]. None of these hypotheses can completely explain the pathological changes seen in KBD. The detailed mechanisms involved in the mitochondrial dysfunction and apoptosis underlying the cartilage lesions in KBD remained unclear

Methods

Results

Conclusion