Keratocyte differentiation

Keratocyte differentiation is a complex biological process rather than a single molecular target. It involves the transformation of quiescent corneal keratocytes into active fibroblasts and, subsequently, alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts, primarily driven by transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) signaling pathways (PMID: 25277150). While keratocytes are essential for maintaining corneal transparency and synthesizing the extracellular matrix, their differentiation into myofibroblasts is a hallmark of the corneal wound healing response following injury, infection, or refractive surgery (PMID: 30894411). Excessive or persistent differentiation leads to the accumulation of disorganized collagen and opaque proteins, resulting in corneal scarring and vision loss (PMID: 28407317). From a therapeutic perspective, 'Keratocyte differentiation' is often viewed as a phenotypic target for preventing corneal haze and fibrosis. Pharmacological intervention frequently focuses on inhibiting the TGF-beta/Smad signaling axis or using antimetabolites like Mitomycin C to limit the population of myofibroblasts during the healing process (PMID: 21862318). Current research also explores the use of small molecule inhibitors and gene therapy to modulate this transition without compromising the cornea's structural integrity or regenerative capacity (PMID: 33502047).

Other names

Keratocyte-to-myofibroblast transitionCorneal stromal cell differentiationKMT

Drugs targeting this process typically inhibit TGF-beta signaling pathways, reduce fibroblast proliferation, or induce apoptosis in myofibroblasts to prevent corneal fibrosis.