Evidence map›Paper›PMID 36193071›Full record

ArticleOxidative medicine and cellular longevity2022

Mitochondria-Targeted Antioxidant Mitoquinone Maintains Mitochondrial Homeostasis through the Sirt3-Dependent Pathway to Mitigate Oxidative Damage Caused by Renal Ischemia/Reperfusion.

Hu Mao, Ye Zhang, Yufeng Xiong, Zijing Zhu, Lei Wang, Xiuheng Liu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  9. The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025
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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

6 authors at 1 institution in 1 country.

Hu MaoDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0003-2252-5572
Ye ZhangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0001-9945-6777
Yufeng XiongDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0001-9810-1691
Zijing ZhuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0003-2615-3040
Lei WangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0001-8412-1130
Xiuheng LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China.ORCID https://orcid.org/0000-0003-3882-2715
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is a critical factor contributing to oxidative stress and apoptosis in ischemia-reperfusion (I/R) diseases. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant whose potent anti-I/R injury capacity has been demonstrated in organs such as the heart and the intestine. In the present study, we explored the role of MitoQ in maintaining mitochondrial homeostasis and attenuating oxidative damage in renal I/R injury. We discovered that the decreased renal function and pathological damage caused by renal I/R injury were significantly ameliorated by MitoQ. MitoQ markedly reversed mitochondrial damage after I/R injury and inhibited renal reactive oxygen species production. In vitro, hypoxia/reoxygenation resulted in increased mitochondrial fission and decreased mitochondrial fusion in human renal tubular epithelial cells (HK-2), which were partially prevented by MitoQ. MitoQ treatment inhibited oxidative stress and reduced apoptosis in HK-2 cells by restoring mitochondrial membrane potential, promoting ATP production, and facilitating mitochondrial fusion. Deeply, renal I/R injury led to a decreased expression of sirtuin-3 (Sirt3), which was recovered by MitoQ. Moreover, the inhibition of Sirt3 partially eliminated the protective effect of MitoQ on mitochondria and increased oxidative damage. Overall, our data demonstrate a mitochondrial protective effect of MitoQ, which raises the possibility of MitoQ as a novel therapy for renal I/R.

Indexed as

Kidney DiseasesReperfusion InjurySirtuin 3Adenosine TriphosphateAntioxidantsHomeostasisHumansIschemiaMitochondriaOrganophosphorus CompoundsOxidative StressReactive Oxygen SpeciesReperfusionUbiquinoneAdenosine TriphosphateAntioxidantsmitoquinoneOrganophosphorus CompoundsReactive Oxygen SpeciesSIRT3 protein, humanSirtuin 3Ubiquinone

Identifiers

PMID36193071
PMCPMC9526615
OpenAlexW4296482075

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.