High Altitude Related Diseases: Milder Effects, HACE, HAPE, and Effect on Various Organ Systems

Singh, Sneha; Ansari, Mairaj Ahmed

doi:10.1007/978-981-19-1008-1_3

Cited by 1 publication

(1 citation statement)

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“…Despite the inherent risks associated with exposure to high altitude hypoxia, mountaineers are drawn to the breathtaking scenery and the physical and mental challenges presented by these environments. Climbing to high altitudes can lead to exposure to hypoxia, which may result in severe neurological dysfunction such as cognitive impairment, memory loss, and even life-threatening conditions such as high-altitude cerebral edema (HACE) and high-altitude pulmonary edema (HAPE) ( Singh and Ansari, 2022 ). Epidemiological studies and laboratory studies have confirmed that acute exposure to high altitude can contribute to neurological decline ( Limmer and Platen, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Sestrin2 protects against hypoxic nerve injury by regulating mitophagy through SESN2/AMPK pathway

Pan,

Ai,

Liang

et al. 2023

Front. Mol. Biosci.

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Hypoxia induced by high altitude can lead to severe neurological dysfunction. Mitophagy is known to play a crucial role in hypoxic nerve injury. However, the regulatory mechanism of mitophagy during this injury remains unclear. Recent studies have highlighted the role of Sestrin2 (SESN2), an evolutionarily conserved stress-inducible protein against acute hypoxia. Our study demonstrated that hypoxia treatment increased SESN2 expression and activated mitophagy in PC12 cells. Furthermore, the knock-out of Sesn2 gene led to a significant increase in mitochondrial membrane potential and ATP concentrations, which protected the PC12 cells from hypoxic injury. Although the AMPK/mTOR pathway was significantly altered under hypoxia, it does not seem to participate in mitophagy regulation. Instead, our data suggest that the mitophagy receptor FUNDC1 plays a vital role in hypoxia-induced mitophagy. Moreover, SESN2 may function through synergistic regulation with other pathways, such as SESN2/AMPK, to mediate cellular adaptation to hypoxia, including the regulation of mitophagy in neuron cells. Therefore, SESN2 plays a critical role in regulating neural cell response to hypoxia. These findings offer valuable insights into the underlying molecular mechanisms governing the regulation of mitophagy under hypoxia and further highlight the potential of SESN2 as a promising therapeutic target for hypoxic nerve injury.

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Section: Introductionmentioning

confidence: 99%