Autophagy is a cellular process wherein cytoplasmic components are sequestered in double-membrane vesicles (autophagosomes) and delivered to lysosomes. In the context of cell injury, autophagy primarily serves as:
- A A pro-apoptotic pathway that constitutively activates caspases
- B A survival mechanism that provides nutrients during starvation and removes damaged organelles ✓
- C A mechanism of immune evasion by sequestering MHC-I antigens
- D An exclusively pro-death pathway analogous to programmed necrosis
Explanation
Autophagy is primarily a cytoprotective and homeostatic process: during nutrient deprivation it degrades cytoplasmic contents to recycle amino acids and energy substrates; it also removes damaged organelles (mitophagy) and misfolded proteins, preventing proteotoxic stress. While excessive autophagy can contribute to cell death, its primary physiological role is survival and cellular quality control. It is initiated by mTOR inhibition under nutrient-poor conditions.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.