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The corneal extracellular matrix (ECM) and cellular microenvironment represent a complex, highly organized structural system essential for ocular transparency and refractive power [1]. The stroma, which comprises about 90% of the corneal thickness, is composed of a precise lattice of Type I and Type V collagen fibrils interspersed with keratan sulfate proteoglycans like lumican and keratocan that maintain fibrillar spacing [2]. Quiescent keratocytes reside within this matrix, playing a critical role in maintaining the ECM through a delicate balance of synthesis and degradation [3]. Pathological alterations in this microenvironment, such as the loss of collagen organization or the transformation of keratocytes into myofibroblasts, lead to conditions like keratoconus and corneal scarring [4]. Therapeutic interventions often target this environment directly, such as riboflavin-mediated collagen cross-linking to increase mechanical stability or the use of TGF-beta inhibitors to prevent fibrotic responses [5]. Understanding the biomechanical and biochemical cues within this niche is vital for developing regenerative therapies and bioengineered corneal substitutes [6]. Citations: [1] Meek, K. M., & Knupp, C. (2015). Progress in Retinal and Eye Research. [2] Hassell, J. R., & Birk, D. E. (2010). Experimental Eye Research. [3] West-Mays, J. A., & Dwivedi, D. J. (2006). Int J Biochem Cell Biol. [4] Torricelli, A. A., et al. (2013). Experimental Eye Research. [5] Wollensak, G., et al. (2003). American Journal of Ophthalmology. [6] Gouveia, A. L., et al. (2019). Biomaterials.
Photo-oxidative collagen cross-linking; TGF-beta pathway inhibition; Rho-kinase inhibition; Proteoglycan synthesis modulation
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