During reperfusion injury after myocardial ischemia, excessive calcium entry into mitochondria opens which channel, triggering loss of inner mitochondrial membrane potential and cell death?
- A Voltage-gated L-type calcium channel
- B IP3 receptor on ER
- C Mitochondrial permeability transition pore (MPTP) ✓
- D Ryanodine receptor (RyR2)
Explanation
During reperfusion, intracellular calcium overload triggers opening of the mitochondrial permeability transition pore (MPTP), a non-selective high-conductance channel in the inner mitochondrial membrane. MPTP opening dissipates the electrochemical gradient needed for ATP synthesis, leads to mitochondrial swelling, outer membrane rupture, cytochrome c release, and execution of both necrotic and apoptotic cell death. This is a major mediator of reperfusion-induced cardiomyocyte death beyond ischemia itself.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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