Fibrosis is a pathological process characterized by the excessive accumulation of extracellular matrix (ECM), particularly collagen, leading to tissue scarring, architectural distortion, and organ dysfunction. While fibrosis is a physiological component of wound healing, its persistence and dysregulation can drive chronic tissue damage and organ dysfunction. In autoimmune diseases, fibrosis arises from prolonged inflammation and immune system dysregulation, creating a vicious cycle that exacerbates tissue injury and promotes disease progression. This review provides a comprehensive overview of the fibrotic processes across a range of immune-mediated and autoimmune conditions, including systemic sclerosis (SSc), morphea, autoimmune hepatitis (AIH), systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS), inflammatory bowel disease (IBD), and rheumatoid arthritis (RA), Finally, we discuss current and emerging antifibrotic strategies aimed at interrupting pathological ECM remodeling and restoring tissue homeostasis.
Żurawek et al. (Sat,) studied this question.
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