Epithelial cell apoptosis-related pathways

Epithelial cell apoptosis-related pathways encompass the complex signaling networks that regulate programmed cell death in epithelial tissues, which serve as critical barriers in the body (Elmore, 2007). These pathways include the intrinsic (mitochondrial) pathway, triggered by internal cellular stress, and the extrinsic (death receptor) pathway, activated by external ligands like TNF-alpha or FASL (Rock and Kono, 2008). In healthy tissues, these pathways maintain homeostasis by removing damaged or redundant cells; however, their dysregulation is a hallmark of various diseases. For instance, excessive apoptosis of lung or intestinal epithelial cells contributes to inflammatory diseases and organ injury, while the evasion of apoptosis is a fundamental driver of epithelial-derived cancers or carcinomas (Guicciardi and Gores, 2009). Therapeutic strategies often focus on specific molecular components within these pathways, such as BCL-2 inhibitors to promote apoptosis in cancer or caspase inhibitors to prevent tissue damage in inflammatory conditions. Monitoring these pathways in clinical settings often involves measuring epithelial-specific biomarkers like the M30 neo-epitope of cytokeratin 18, which is released during apoptotic cleavage (Kramer et al., 2004).

Other names

Epithelial apoptosis signalingProgrammed cell death in epitheliumEpithelial cell death pathways

Modulation of specific apoptotic signaling components, such as inhibiting anti-apoptotic BCL-2 family proteins to promote cell death in oncology or inhibiting caspases to prevent pathological cell loss in inflammatory diseases (Fuchs and Steller, 2011).