2.3 Cell Death: Apoptosis and Necrosis

Cell death mechanisms are crucial for understanding how our bodies maintain balance and respond to injury. Apoptosis, a controlled process, helps shape organs and regulate the immune system. Necrosis, an uncontrolled death, occurs from severe damage like burns or toxins.

These processes play vital roles in health and disease. Dysregulated cell death contributes to cancer, neurodegenerative diseases, and autoimmune disorders. Understanding these mechanisms is key for developing treatments targeting apoptotic pathways or preventing excessive necrosis in various conditions.

Cell Death Mechanisms

Apoptosis vs necrosis

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• Apoptosis involves programmed cell death maintaining tissue homeostasis through controlled energy-dependent process characterized by cell shrinkage and fragmentation (embryonic development)
• Necrosis occurs as accidental or uncontrolled cell death resulting from external factors often caused by severe cellular injury characterized by cell swelling and rupture (severe burns)

Molecular mechanisms of apoptosis

• Extrinsic pathway activated by external death ligands involving death receptors (Fas, TNF receptor) leads to activation of initiator caspases (caspase-8 or -10)
• Intrinsic pathway triggered by internal cellular stress involves mitochondrial outer membrane permeabilization releasing cytochrome c into cytosol forming apoptosome activating initiator caspase-9
• Execution phase activates effector caspases (caspase-3, -6, and -7) cleaving cellular proteins fragmenting DNA forming apoptotic bodies

Physiological roles of apoptosis

• Embryonic development removes unnecessary cells during organ formation shaping limbs and digits forming neural tube (webbed fingers)
• Immune system regulation eliminates self-reactive lymphocytes terminates immune responses maintains peripheral tolerance (autoimmune prevention)
• Tissue homeostasis balances cell proliferation and death removing damaged or potentially harmful cells (skin cell turnover)

Characteristics and causes of necrosis

• Morphological characteristics include cell swelling plasma membrane rupture release of cellular contents inflammation in surrounding tissue (tissue edema)
• Biochemical characteristics involve ATP depletion loss of ion homeostasis activation of degradative enzymes oxidative stress (cellular energy crisis)
• Potential causes encompass ischemia or hypoxia toxins or poisons extreme temperature changes mechanical trauma infections (frostbite)

Dysregulated cell death in disease

• Cancer exhibits reduced apoptosis leading to uncontrolled cell growth mutations in pro-apoptotic genes (p53) overexpression of anti-apoptotic proteins (Bcl-2)
• Neurodegenerative diseases show excessive apoptosis in Alzheimer's and Parkinson's diseases accumulation of misfolded proteins triggering cell death mitochondrial dysfunction leading to neuronal loss
• Autoimmune disorders fail to eliminate self-reactive lymphocytes increase resistance to apoptosis in autoreactive cells (lupus)
• Ischemic injuries cause necrosis in heart attacks and strokes secondary damage due to inflammation (myocardial infarction)
• Therapeutic implications include targeting apoptotic pathways in cancer treatment developing neuroprotective strategies for neurodegenerative diseases (chemotherapy)