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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Fibrosis--a lethal component of systemic sclerosis.

Yuen Yee Ho1, David Lagares2, Andrew M Tager2

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Systemic sclerosis (SSc) involves progressive fibrosis, a major cause of death in rheumatic diseases. This review explores fibrosis initiation and progression in SSc, highlighting potential therapeutic targets.

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Area of Science:

  • Pathology
  • Rheumatology
  • Fibrosis Research

Background:

  • Fibrosis, excessive connective tissue accumulation, stems from deregulated wound healing in response to chronic injury or inflammation.
  • In systemic sclerosis (SSc), progressive fibrosis distorts tissue architecture, leading to significant organ dysfunction, morbidity, and mortality.
  • Fibrosis is a key pathological process in rheumatic diseases, particularly SSc.

Purpose of the Study:

  • To review the pathological role of fibrosis in systemic sclerosis (SSc).
  • To elucidate the initiating factors and progression mechanisms of fibrosis in SSc.
  • To identify potential therapeutic targets for SSc-related fibrosis.

Main Methods:

  • Review of literature on fibrosis in systemic sclerosis.
  • Discussion of cellular and molecular mechanisms involved in fibrosis initiation and progression.
  • Analysis of signaling pathways driving fibroblast activation and myofibroblast differentiation.

Main Results:

  • Fibrosis in SSc is initiated by endothelium and pericyte activation, immune responses, endoplasmic reticulum stress, and chronic tissue injury.
  • Fibroblast activation and myofibroblast differentiation lead to excessive extracellular matrix accumulation.
  • Chemical and mechanical signals critically drive these fibrotic processes.

Conclusions:

  • Understanding the multifaceted mechanisms of fibrosis in SSc is crucial for developing effective treatments.
  • Targeting initiating factors, fibroblast activation, and matrix accumulation pathways offers potential therapeutic strategies for SSc.
  • Further research into the chemical and mechanical signals driving fibrosis may lead to novel therapies for systemic sclerosis.