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Updated: Oct 15, 2025

Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients
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Generation of Induced-pluripotent Stem Cells Using Fibroblast-like Synoviocytes Isolated from Joints of Rheumatoid Arthritis Patients

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New potential therapeutic approaches targeting synovial fibroblasts in rheumatoid arthritis

María José Alcaraz1

  • 1Department of Pharmacology, University of Valencia, and Interuniversity Research Institute for Molecular Recognition and Technological Development (IDM), Polytechnic University of Valencia, University of Valencia, Av. Vicent A. Estellés s/n, 46100 Burjasot, Valencia, Spain.

Biochemical Pharmacology
|October 29, 2021
PubMed

Insights

Activated synovial fibroblasts drive joint destruction in rheumatoid arthritis (RA). Targeting these cells offers a promising strategy for novel RA therapeutics to preserve joint function.

Area of Science:

  • Rheumatology
  • Cell Biology
  • Immunology

Background:

  • Synovial fibroblasts (SFs) are key drivers of joint destruction in chronic inflammatory conditions.
  • Activated SFs in rheumatoid arthritis (RA) adopt an aggressive phenotype, causing cartilage degradation and bone erosion.

Purpose of the Study:

  • To review the role of SFs in RA pathogenesis.
  • To explore SFs as a therapeutic target for preserving joint architecture and function in RA.

Main Methods:

  • Literature review of recent research on SFs in RA.
  • Analysis of potential therapeutic strategies targeting SF phenotypes, epigenetic changes, cellular functions, and signaling pathways.

Main Results:

  • Various approaches targeting SFs have shown efficacy in preclinical models.
  • Identification and modulation of SF phenotypes are crucial for controlling arthritogenic changes.
  • Regulation of cation channels and signaling pathways in SFs are potential therapeutic avenues.

Conclusions:

  • SFs represent a significant therapeutic target for developing novel RA treatments.
  • Further research is necessary to identify the most effective targets for drug development to preserve joint integrity in RA.
Keywords:
ApoptosisDrug targetInflammationRheumatoid arthritisSignal transductionSynovial fibroblast

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