Single-cell and bulk tissue sequencing unravels the heterogeneity of synovial microenvironment in arthrofibrosis

Chen, Xi; Gong, Li-Hua; Li, Cheng; Wang, Siyuan; Wang, Ziyuan; Chu, Ming; Zhou, Yixin

doi:10.1016/j.isci.2023.107379

Cited by 1 publication

(2 citation statements)

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“…In addition, the study conducted by Chen et al. revealed a distinctive trajectory in DKK3 + FLS within the sublining layer, transitioning from fibroblasts to myofibroblasts ( 83 ). This finding implies a possible link between the activation of the DKK3 subpopulation and the differentiation process leading to myofibroblasts in OA ( 83 ).…”

Section: The Diversity Of Phenotypes and Functions Of Fibroblastmentioning

confidence: 99%

“…revealed a distinctive trajectory in DKK3 + FLS within the sublining layer, transitioning from fibroblasts to myofibroblasts ( 83 ). This finding implies a possible link between the activation of the DKK3 subpopulation and the differentiation process leading to myofibroblasts in OA ( 83 ). However, further studies are needed to investigate the role of fibroblast subsets in synovial tissue fibrosis and to identify their characteristic phenotype.…”

Section: The Diversity Of Phenotypes and Functions Of Fibroblastmentioning

confidence: 99%

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Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis

Damerau,

Rosenow,

Alkhoury

et al. 2024

Front. Immunol.

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Osteoarthritis (OA) is the most common form of arthritis, characterized by osteophyte formation, cartilage degradation, and structural and cellular alterations of the synovial membrane. Activated fibroblast-like synoviocytes (FLS) of the synovial membrane have been identified as key drivers, secreting humoral mediators that maintain inflammatory processes, proteases that cause cartilage and bone destruction, and factors that drive fibrotic processes. In normal tissue repair, fibrotic processes are terminated after the damage has been repaired. In fibrosis, tissue remodeling and wound healing are exaggerated and prolonged. Various stressors, including aging, joint instability, and inflammation, lead to structural damage of the joint and micro lesions within the synovial tissue. One result is the reduced production of synovial fluid (lubricants), which reduces the lubricity of the cartilage areas, leading to cartilage damage. In the synovial tissue, a wound-healing cascade is initiated by activating macrophages, Th2 cells, and FLS. The latter can be divided into two major populations. The destructive thymocyte differentiation antigen (THY)1─ phenotype is restricted to the synovial lining layer. In contrast, the THY1+ phenotype of the sublining layer is classified as an invasive one with immune effector function driving synovitis. The exact mechanisms involved in the transition of fibroblasts into a myofibroblast-like phenotype that drives fibrosis remain unclear. The review provides an overview of the phenotypes and spatial distribution of FLS in the synovial membrane of OA, describes the mechanisms of fibroblast into myofibroblast activation, and the metabolic alterations of myofibroblast-like cells.

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Section: The Diversity Of Phenotypes and Functions Of Fibroblastmentioning

confidence: 99%

Section: The Diversity Of Phenotypes and Functions Of Fibroblastmentioning

confidence: 99%