Cellular death results from oxygen deprivation due to the failure of aerobic ATP production
Oxygen deprivation and subsequent failure of aerobic ATP production trigger critical mitochondrial dysfunction and energetic collapse, which are primary drivers of cellular death in ischemic and hypoxic injuries.
The retrieved papers consistently establish that cellular death during ischemic and hypoxic conditions is strongly mediated by bioenergetic failure, specifically the depletion of ATP resulting from mitochondrial dysfunction induced by oxygen deprivation.
Malaeb S, Grothusen J, Tuzer F, Delivoria-Papadopoulos M. Inhaled nitric oxide and hypoxic brain injury in newborn piglets.. 2026. https://doi.org/10.1016/j.niox.2026.07.003
Demonstrates that hypoxia and subsequent energy metabolic crisis lead to severe cellular and biochemical injury markers.
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Hao G, Bai Z, Wang W, Wu J, Zheng F, Jin G, Ge RL. High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.. 2026. https://doi.org/10.1002/cns.70986
Shows that chronic high-altitude hypoxia drives severe ATP depletion coupled with mitochondrial collapse and cellular apoptosis.
Abueid L, Torun AF, Golal E, Acar N, Basralı F. Renoprotective Effect of S14G-Humanin on Renal Ischemia/Reperfusion Injury by Activation of STAT3 and ERK 1/2 Signal Transduction Pathways in Rats. 2026. https://doi.org/10.21203/rs.3.rs-9040130/v1
Indicates that restoring mitochondrial ATP levels through protective interventions significantly reduces cellular apoptosis and necrosis following ischemic injury.
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