Corneal stromal fibroblast (CSF)

Corneal stromal fibroblasts are activated mesenchymal cells that differentiate from quiescent keratocytes in response to corneal injury, surgery, or inflammation (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590014/). They serve as the primary mediators of the corneal wound healing process, migrating to the site of injury and proliferating to synthesize new extracellular matrix (ECM) components (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9183221/). While their activity is necessary for structural repair, persistent or excessive fibroblast activity—particularly the transition into myofibroblasts—leads to the deposition of disorganized collagen and the formation of light-scattering scars known as corneal haze or fibrosis (ResearchGate, https://www.researchgate.net/publication/366014431_Topical_Losartan_Decreases_Corneal_Scarring_Fibrosis_and_Myofibroblast_Generation_After_PRK_in_Rabbits). Additionally, these cells act as sentinel cells in the cornea, sensing pathogens and releasing chemokines to recruit inflammatory cells during infection (NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590014/). Pharmacological targeting of these cells often involves the use of anti-proliferative agents like mitomycin C or anti-inflammatory steroids to prevent vision-impairing opacity (Journal of Refractive Surgery, https://doi.org/10.3928/1081597X-20170921-02). Modern therapeutic strategies also focus on modulating specific signaling pathways, such as the TGF-beta, Rho-kinase, and IRF3 pathways, to promote regenerative rather than fibrotic healing (ARVO Journals, https://doi.org/10.1167/iovs.67.3.49; NIH, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304400/).

Other names

Activated keratocyteCorneal fibroblastMyofibroblast

Inhibition of DNA synthesis and cell proliferation, suppression of TGF-beta signaling pathways, and modulation of inflammatory cytokine and chemokine expression.