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Apoptotic pathways in limbal stem cells (LSCs) encompass the complex signaling cascades, including the intrinsic mitochondrial and extrinsic death receptor pathways, that regulate programmed cell death in the corneal periphery (Dua et al., 2000 [PMID: 11004112]). LSCs are essential for maintaining the transparency and integrity of the corneal epithelium; their depletion through apoptosis is a primary driver of limbal stem cell deficiency (LSCD) (Ahmad et al., 2010 [PMID: 20634901]). This condition is characterized by conjunctivalization, neovascularization, and chronic inflammation, often resulting from chemical burns, UV damage, or autoimmune disorders. Therapeutic strategies targeting these pathways aim to inhibit pro-apoptotic factors like Caspase-3 and Bax while promoting survival signals such as Bcl-2 and the PI3K/Akt pathway (Polisetti et al., 2016 [PMID: 27154321]). Understanding these mechanisms is crucial for developing regenerative therapies and pharmacological interventions, such as growth factors or anti-inflammatory agents, to preserve the ocular surface niche (Chen et al., 2010 [PMID: 20154256]).
Modulation of the balance between pro-apoptotic and anti-apoptotic protein expression to preserve the limbal stem cell niche and prevent corneal epithelial failure.
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