Apoptosis-related proteins and pathways

Apoptosis-related proteins and pathways encompass the complex molecular machinery responsible for programmed cell death, a critical process for maintaining cellular homeostasis and eliminating damaged or redundant cells [Elmore, 2007]. This network is primarily categorized into the intrinsic (mitochondrial) pathway, regulated by the Bcl-2 family of proteins, and the extrinsic (death receptor) pathway, triggered by external ligands such as TNF-alpha or FASL [NIH; StatPearls]. Both pathways converge on the activation of caspases, which are cysteine proteases that execute cell death by cleaving specific cellular substrates [UniProt]. Dysregulation of these pathways is a hallmark of various diseases; for instance, evasion of apoptosis is a core feature of cancer, while excessive apoptosis contributes to neurodegenerative and cardiovascular disorders [Hanahan & Weinberg, 2011; StatPearls]. Therapeutic strategies often focus on restoring apoptotic sensitivity in cancer cells using BH3 mimetics or IAP inhibitors, or inhibiting cell death in degenerative conditions [PubChem]. Because this term refers to a broad biological process rather than a single molecular entity, it is considered a pathway or category rather than a specific therapeutic target.

Other names

Programmed cell death pathwaysApoptotic signaling cascadeCell death machineryApoptosome-related pathways

Drugs targeting these pathways function by either inhibiting anti-apoptotic proteins (e.g., Bcl-2, Mcl-1) to trigger the intrinsic pathway, or by activating pro-apoptotic receptors and enzymes (e.g., Caspases, TRAIL receptors) to induce cell death in target populations like tumor cells [Elmore, 2007; PubChem].