
IL-6 신호 전달은 건 조직의 수리 섬유아세포 활성화와 손상 부위로의 이동을 촉진하여 건 질환의 주요 특징을 악화시킨다.


coremsg

Tendinopathies are debilitating diseases currently increasing in prevalence and associated costs. There is a need to deepen our understanding of the underlying cell signaling pathways to unlock effective treatments. In this work, we screen cell signaling pathways in human tendinopathies and find positively enriched IL-6/JAK/STAT signaling alongside signatures of cell populations typically activated by IL-6 in other tissues. In human tendinopathic tendons, we also confirm the strong presence and co-localization of IL-6, IL6R, and CD90, an established marker of reparative fibroblasts. To dissect the underlying causalities, we combine IL-6 knock-out mice with an explant-based assembloid model of tendon damage to successfully connect IL-6 signaling to reparative fibroblast activation and recruitment. Vice versa, we show that these reparative fibroblasts promote the development of tendinopathy hallmarks in the damaged explant upon IL-6 activation. We conclude that IL-6 activates tendon fibroblast populations which then initiate and deteriorate tendinopathy hallmarks.

### Competing Interest Statement

The authors have declared no competing interest.

IL-6 SIGNALING EXACERBATES HALLMARKS OF CHRONIC TENDON DISEASE BY STIMULATING REPARATIVE FIBROBLASTS

만성-건-질환의-주요-특징을-악화시키는-il-6-신호-전달-전구체-증식-및-손상-부위로의-이동-촉진


만성 건 질환의 주요 특징을 악화시키는 IL-6 신호 전달: 전구체 증식 및 손상 부위로의 이동 촉진
