Cell Injury and Its Consequences
Cell Death: Apoptosis and Necrosis
Cell injury triggers two forms of cell death: apoptosis, a controlled process, and necrosis, an unregulated response to extreme damage. These mechanisms play a crucial role in disease pathology and treatment strategies.
Cell Injury and Its Consequences
Cell Death: Apoptosis and Necrosis
Cells encounter various forms of stress, and their response determines their survival or demise. When damage exceeds the repair threshold, cells undergo either apoptosis or necrosis.
Apoptosis: Programmed Cell Death
Apoptosis is a tightly regulated, energy-dependent process that eliminates unwanted or damaged cells without inducing inflammation.
- Intrinsic pathway: Mitochondrial-mediated death triggered by DNA damage.
- Extrinsic pathway: Death receptor signaling leading to caspase activation.
- Cellular features: Nuclear fragmentation, cytoplasmic shrinkage, and apoptotic body formation.
Necrosis: Unregulated Cell Death
Unlike apoptosis, necrosis occurs due to severe cellular damage and is accompanied by inflammation.
- Causes: Hypoxia, toxins, infections, and trauma.
- Cellular features: Cell swelling, membrane rupture, and enzymatic digestion.
- Types: Coagulative necrosis (seen in ischemia), liquefactive necrosis (common in brain infarcts), and caseous necrosis (tuberculosis).
Clinical Significance
Understanding apoptosis and necrosis aids in diagnosing diseases such as cancer, neurodegeneration, and autoimmune disorders. Targeting apoptotic pathways forms the basis of many therapeutic interventions.
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