Ning Yujie, Wang Xi, Zhang Pan, Liu Amin, Qi Xin, Liu Meidan, Guo Xiong
Institute of Endemic Diseases, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, P.R. China.
Exp Ther Med. 2018 Apr;15(4):3680-3686. doi: 10.3892/etm.2018.5885. Epub 2018 Feb 22.
Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit β, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD.
以往的研究已经确定了饮食与大骨节病(KBD)患病率之间的密切关联;然而,饮食预防KBD相关软骨损伤的机制仍不清楚。最近的国际研究揭示了饮食外泌体微小(mi)RNA通过调节与细胞凋亡和细胞外基质相关的基因和蛋白质在修复软骨细胞损伤中的治疗作用。初步确定,影响软骨细胞生物功能的重要分子,包括miR-23b和蛋白激酶环磷酸腺苷激活催化亚基β,在KBD患者的细胞和软骨组织中表达失调。饮食外泌体在KBD软骨细胞损伤修复中的作用是该领域的一个新课题。值得探讨饮食外泌体-miR-23b通过调节蛋白激酶A(PKA)信号通路对软骨细胞损伤的保护作用。以下目标在未来的研究中具有重要意义:i)验证外泌体与KBD患者软骨损伤之间的关联;ii)确定miR-23b在软骨损伤中的保护机制是否通过调节PKA途径进行;iii)探索饮食外泌体-miR-23b在修复环境危险因素诱导的软骨细胞损伤中的治疗作用。这些想法可能有助于在分子、细胞和机体水平上确立饮食外泌体-miR-23b在修复软骨细胞损伤中的治疗作用和机制。这些研究可能同时阐明疾病发病机制,并为KBD的新型生物标志物和治疗方法提供证据。