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This study found that in rheumatoid arthritis patients, inflammatory macrophages activate steroid metabolism to increase glucocorticoid and androgen production, which helps suppress inflammation and attenuate hyperproliferation in synovial fibroblasts, with notable disturbances seen in postmenopausal women due to diminished inactive steroid precursors.

In this study, researchers found that the compound BMS-470539 induced a senescence-like state in fibroblasts from systemic sclerosis patients, reducing fibrosis-associated markers in vitro and decreasing skin thickness in a mouse model of skin fibrosis, suggesting a novel therapeutic strategy for managing fibroblast-driven diseases.

This study reports that in systemic sclerosis, CD34+ dermal fibroblasts transition to CD34−, podoplanin+, and CD90+ fibroblasts across the dermis, suggesting a role in unchecked fibrosis.

This study identified CD201+ fibroblast progenitors in mouse skin that regulate wound healing through differentiation into specialized cell types, with retinoic acid and hypoxia influencing this process.

This study found that platelet-rich growth factor significantly reduced the release of proinflammatory cytokines in an in vitro rheumatoid arthritis model.