ORIGINAL RESEARCH article
Front. Physiol.
Sec. Clinical and Translational Physiology
Effects of Mitochondrial Gene Mutation 8923 (A→G) on Inflammatory Indicators and Blood Pressure after Acute High-Altitude Exposure
Minglei Zhang 1,2
Ruizhe Li 3
Yining Liu 2
Zongbin Li 1,2,3
1. Sixth Medical Center of PLA General Hospital, Beijing, China
2. Nankai University School of Medicine, Tianjin, China
3. Chinese PLA Medical College, Chinese PLA General Hospital, Beijing, China
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Abstract
Background: In recent years, an increasing number of individuals have traveled to or resided in plateau regions for various reasons. The hypobaric hypoxia characteristics of plateau environments represents a key risk factor for acute mountain sickness (AMS). The pathogenesis of AMS remains incompletely understood. The present study aimed to explore the association between the A8923G point mutation in the mitochondrial MT-ATP6 gene and AMS. Methods: We enrolled 84 healthy adult male volunteers who traveled together from the plain (Beijing, <100 m) to a 4000-m plateau in <40 hours. Peripheral venous blood was collected for related tests; volunteers also underwent ambulatory blood pressure/electrocardiography monitoring. We analyzed these physiological indicators to examine the association between the MT-ATP6 A8923G mutation and AMS. Results: After acute high-altitude exposure, the mutation group had lower C-reactive protein (CRP) [0.04(0.03,0.04) vs. 0.07(0.03.0.13), P =0.045] and higher high-density lipoprotein cholesterol (HDL-C) [1.5±0.4 vs. 1.3±0.3, P =0.021] than the non-mutation group, plus lower 24-hour and nocturnal mean systolic blood pressure (SBP) (all P <0.05), with significant intergroup differences. Conclusions: The A8923G point mutation acts as a protective locus against AMS. It was associated with lower high-altitude SBP (more pronounced at night), reduced CRP and elevated HDL-C, possibly by inhibiting inflammation and enhancing blood pressure regulation post high-altitude exposure.
Summary
Keywords
Blood Pressure, clinical, gene mutation, Inflammatory indicators, mitochondrial
Received
29 December 2025
Accepted
19 February 2026
Copyright
© 2026 Zhang, Li, Liu and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Zongbin Li
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