Stress proteins actively sustain joint inflammation in osteoarthritis, study finds
Why do some joints remain chronically inflamed in osteoarthritis and other rheumatic diseases? Researchers have taken an important step toward answering this question. Their findings, published in the journal Cell Death & Differentiation, highlight the key role of proteins associated with endoplasmic reticulum (ER) stress, a cellular mechanism that has so far been only sparsely investigated in…
Researchers have discovered that specific proteins, triggered by endoplasmic reticulum (ER) stress, actively sustain joint inflammation in osteoarthritis. Published in Cell Death & Differentiation, the study, conducted by a team at the Rheumatology Laboratory of the University of Liège, reveals the critical role of these proteins in the progression of synovitis, the inflammation of the synovial membrane that lines joints.
Synovial membrane, a key player in inflammatory processes, is analyzed for the first time in human joint tissues, providing insight into the molecular mechanisms driving joint inflammation. The research highlights the increase of ER stress proteins in synovial membranes as inflammation advances, particularly in fibroblast-like synoviocytes (FLS), cells implicated in tissue remodeling and joint damage.
Among the proteins examined, PDIA4 emerged as a potential therapeutic target due to its suppression leading to reduced proliferation and migration of fibroblast-like synoviocytes. By identifying these ER stress proteins and their roles, the study paves the way for more targeted therapies to mitigate the inflammatory and tissue-destructive processes in joint diseases.
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