Carpintero-Fernández Paula, Varela-Eirín Marta, García-Yuste Alejandro, López-Díaz Iñaki, Caeiro José Ramón, Mayán María D
CellCOM Research Group, Instituto de Investigación Biomédica de A Coruña (INIBIC), Servizo Galego de Saúde (SERGAS), Universidade da Coruña (UDC), A Coruña, Spain.
European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), Groningen, The Netherlands.
Bioelectricity. 2022 Mar 15;4(1):39-47. doi: 10.1089/bioe.2021.0039. eCollection 2022 Mar.
Osteoarthritis (OA) is the most common joint disease. In the last years, the research community has focused on understanding the molecular mechanisms that led to the pathogenesis of the disease, trying to identify different molecular and clinical phenotypes along with the discovery of new therapeutic opportunities. Different types of cell-to-cell communication mechanisms have been proposed to contribute to OA progression, including mechanisms mediated by connexin43 (Cx43) channels or by small extracellular vesicles. Furthermore, changes in the chondrocyte phenotype such as cellular senescence have been proposed as new contributors of the OA progression, changing the paradigm of the disease. The use of different drugs able to restore chondrocyte phenotype, to reduce cellular senescence and senescence-associated secretory phenotype components, and to modulate ion channel activity or Cx43 appears to be promising therapeutic strategies for the different types of OA. In this review, we aim to summarize the current knowledge in OA phenotypes related with aging and tissue damage and the new therapeutic opportunities currently available.
骨关节炎（OA）是最常见的关节疾病。在过去几年中，研究界一直专注于了解导致该疾病发病机制的分子机制，试图识别不同的分子和临床表型，并发现新的治疗机会。已经提出了不同类型的细胞间通讯机制促进骨关节炎的进展，包括由连接蛋白43（Cx43）通道或小细胞外囊泡介导的机制。此外，软骨细胞表型的变化，如细胞衰老，被认为是骨关节炎进展的新因素，改变了该疾病的范式。使用不同的药物来恢复软骨细胞表型、减少细胞衰老和衰老相关分泌表型成分，以及调节离子通道活性或Cx43，似乎是针对不同类型骨关节炎的有前景的治疗策略。在这篇综述中，我们旨在总结与衰老和组织损伤相关的骨关节炎表型的当前知识以及目前可用的新治疗机会。
