Explains apoptosis as programmed cell death, listing its morphological features and its roles in development, immunity and cancer prevention. It then sets out the intrinsic mitochondrial and extrinsic death-receptor pathways, the execution phase, and the regulators Bcl-2 family proteins, IAPs, p53 and NF-κB. Clinical links to cancer, autoimmunity, neurodegeneration and infection follow, with four multiple-choice questions and answers at the end.
Topic 60 of 70 in the MU Sofia syllabus for Biochemistry (Medicine, Year 2). The free AceMed note covers it in 8 sections, about 574 words (4 min of reading), with 10 flashcards.
In this note
Apoptosis: Molecular Mechanisms and Biological Role
Biological Role of Apoptosis
Molecular Mechanisms of Apoptosis
Execution Phase
Regulation of Apoptosis
Clinical Significance of Apoptosis
MCQs
Answers
Apoptosis: Molecular Mechanisms and Biological Role
Overview of Apoptosis
Definition: Apoptosis is a form of programmed cell death that is essential for the development and maintenance of healthy tissues.
Characteristics:
Cell Shrinkage: Reduction in cell size.
Chromatin Condensation: DNA condenses and fragments.
Membrane Blebbing: Cell membrane forms bulges.
Formation of Apoptotic Bodies: Cell breaks into smaller, membrane-bound fragments.
Phagocytosis: Apoptotic bodies are engulfed and digested by phagocytes.
Biological Role of Apoptosis
Development:
Embryogenesis: Removal of unnecessary cells during development.
Tissue Homeostasis: Balances cell proliferation and death to maintain tissue integrity.
Immune System:
Elimination of Infected Cells: Removal of cells infected by viruses or other pathogens.
Self-Tolerance: Deletion of self-reactive immune cells to prevent autoimmunity.
Disease Prevention:
Cancer Prevention: Elimination of damaged or potentially cancerous cells.
Molecular Mechanisms of Apoptosis
Pathways of Apoptosis
Intrinsic Pathway (Mitochondrial Pathway):
Trigger: Internal stress signals (e.g., DNA damage, oxidative stress).
Key Players:
Bcl-2 Family Proteins: Regulate mitochondrial outer membrane permeability.
Cytochrome c: Released from mitochondria into the cytoplasm.
Apaf-1: Binds cytochrome c and forms the apoptosome.
Caspase-9: Activated by the apoptosome to initiate caspase cascade.
Outcome: Activation of executioner caspases (e.g., caspase-3) leading to apoptosis.
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