Evidence map›Paper›PMID 24498190›Full record

ArticlePloS one2014

Mitochondrial DNA 10609T promotes hypoxia-induced increase of intracellular ROS and is a risk factor of high altitude polycythemia.

Chunhua Jiang, Jianhua Cui, Fuyu Liu, Liang Gao, Yongjun Luo, Peng Li, Libin Guan, Yuqi Gao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Chunhua JiangDepartment of Pathophysiology and High Altitude Physiology, College of High Altitude Military Medicine, Third Military Medical University, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Jianhua CuiResearch Center of PLA for Prevention and Treatment of High Mountain Sickness, the 18th Hospital of PLA, Yecheng, Xinjiang, PR China.
Fuyu LiuKey Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Liang GaoResearch Center of PLA for Prevention and Treatment of High Mountain Sickness, the 18th Hospital of PLA, Yecheng, Xinjiang, PR China.
Yongjun LuoKey Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Peng LiKey Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Libin GuanDepartment of Pathophysiology and High Altitude Physiology, College of High Altitude Military Medicine, Third Military Medical University, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Yuqi GaoDepartment of Pathophysiology and High Altitude Physiology, College of High Altitude Military Medicine, Third Military Medical University, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, Ministry of Education, Chongqing, PR China ; Key Laboratory of High Altitude Medicine, PLA, Chongqing, PR China.
Ministry of Education of the People's Republic of China · CN82th Hospital of Pla · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypobaric hypoxia is the primary cause of high altitude polycythemia (HAPC). Mitochondria are critical organelles that consume high levels of oxygen and generate ATP. We hypothesize that the mitochondrion may be at the center of HAPC, and mitochondrial DNA (mtDNA) SNPs may be involved in its development. First, we conducted a case-control study to investigate the association of mtDNA variants with HAPC in Han Chinese migrating to the Qinghai-Tibetan Plateau. Pearson's chi-square tests revealed that mtDNA 8414T (MU) frequency (19.5%) in the HAPC group was significantly higher than that of the control (13.0%, P = 0.04, OR = 1.615, 95%CI: 1.020-2.555). The multivariate logistic regression analysis, after adjustment for environmental factors, revealed that mtDNA 10609T (WT) was significantly associated with an increased risk of HAPC (P<0.01, OR = 2.558, 95%CI: 1.250-5.236). Second, to verify the association, in vitro experiments of transmitochondrial cybrids was performed and revealed that the mtDNA 10609 variant promoted hypoxia-induced increase of intracellular ROS, but the mtDNA 8414 variant did not. Our findings provide evidence that, in Han Chinese, mtDNA 10609T promotes hypoxia-induced increase of intracellular ROS and is a HAPC risk factor.

Indexed as

AdultAltitudeAltitude SicknessAsian PeopleCase-Control StudiesDNA, MitochondrialHumansHypoxiaMitochondriaPolycythemiaPolymorphism, Single NucleotideReactive Oxygen SpeciesRisk FactorsDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID24498190
PMCPMC3907523
OpenAlexW2062918288

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.