Evaluation of the cell death markers for aberrated cell free DNA release in high altitude pulmonary edema

High-altitude pulmonary edema
DOI: 10.1042/cs20242052 Publication Date: 2024-11-07T17:27:51Z
ABSTRACT
Abstract The effect of high altitude (HA, >2500 m) can trigger a maladaptive response in unacclimatized individuals, leading to various HA illnesses such as pulmonary edema (HAPE). present study investigates circulating cell free (cf) DNA, minimally invasive biomarker that elicit pro-inflammatory response. Our earlier observed altered cfDNA fragment patterns HAPE patients and the significant correlation these with peripheral oxygen saturation levels. However, unclear release mechanisms circulation limit its characterization clinical utility. not only increase levels (27.03 ± 1.37 ng/ml; n = 145) compared healthy sojourners (controls, 14.57 0.74 65) highlanders (HLs, 15.50 0.8 34) but also assayed known death markers involved at HA. found significantly elevated apoptotic marker, annexin A5, secondary necrosis or late mobility group box 1, patients. In addition, we higher oxidative DNA damage 8-hydroxy-2′-deoxyguanosine, controls, suggestive role status promoting inflammatory potential fragments their plausible manifesting pathophysiology. Extensive vitro future assays confirm immunogenic may act danger-associated molecular pattern associate cellular stresses HAPE.
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