Evidence map›Paper›PMID 30431108›Full record

ArticleInternational journal of molecular medicine2019

Mitochondria-targeted antioxidant therapy for an animal model of PCOS-IR.

Yu Ding, Zhaochang Jiang, Bohou Xia, Lizong Zhang, Caijuan Zhang, Jianhang Leng

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  17. Analysis of Mitochondrial Transfer RNA Mutations in Breast Cancer.Balkan journal of medical genetics : BJMG · 2023
    Article
  18. Mitochondrial Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Review
  19. Review
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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 4 institutions in 1 country.

Yu DingCentral Laboratory, Hangzhou First People's Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Zhaochang JiangDepartment of Pathology, Second Affiliated Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Bohou XiaDepartment of Pharmacy, Hunan Chinese Medical University, Changsha, Hunan 410208, P.R. China.
Lizong ZhangDepartment of Experimental Animal Center, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, P.R. China.
Caijuan ZhangDepartment of Gynecological and Obstetrics, Hangzhou First People's Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Jianhang LengCentral Laboratory, Hangzhou First People's Hospital, Zhejiang University, School of Medicine, Hangzhou, Zhejiang 310006, P.R. China.
Hangzhou First People's Hospital · CNHunan University of Traditional Chinese Medicine · CNSecond Affiliated Hospital of Zhejiang University · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder with unknown etiology and unsatisfactory clinical treatment. Considering the ethical limitations of studies involving humans, animal models that reflect features of PCOS and insulin resistance (IR) are crucial resources in investigating this syndrome. Our previous study showed that mitochondrial dysfunction resulted from pathogenic mutations of mitochondrial DNA (mtDNA), and that oxidative stress had an active role in the phenotypic manifestation of PCOS‑IR. Therefore, it was hypothesized that limiting oxidative stress and mitochondrial damage may be useful and effective for the clinical treatment of PCOS‑IR. For this purpose, the present study examined the therapeutic effects of the mitochondria‑targeted antioxidant MitoQ10 for PCOS‑IR. Furthermore, the histopathology was used to analysis the ovarian morphological changes. The endocrine and reproductive related parameters were analyzed by ELISA approach. A PCOS‑IR model was successfully established by subcutaneous injection of rats with testosterone propionate and feeding a high‑fat diet. The 30 female Sprague‑Dawley rats were then divided into three groups, comprising a control (n=10), animal model (PCOS‑IR, n=10) and MitoQ10 treatment (n=10) group. It was found that MitoQ10 significantly improved the IR condition and reversed the endocrine and reproductive conditions of PCOS. In addition, the impaired mitochondrial functions were improved following MitoQ10 administration. Notably, western blot results suggested that this antioxidant reduced the expression levels of apoptosis‑related proteins cytochrome c and B‑cell lymphoma‑2 (Bcl‑2)‑associated X protein, whereas the anti‑apoptotic protein Bcl‑extra large was increased following MitoQ10 treatment. Taken together, the data indicated that the MitoQ10 may have a beneficial favorable therapeutic effect on animals with PCOS‑IR, most likely via the protection of mitochondrial functions and regulation of programmed cell death‑related proteins.

Indexed as

Insulin ResistanceAnimalsAntioxidantsbcl-2-Associated X Proteinbcl-X ProteinBiomarkersCytochromes cDisease Models, AnimalEndocrine SystemFemaleHormonesMitochondriaOxidative StressPolycystic Ovary SyndromeRats, Sprague-DawleyReproductionAntioxidantsbcl-2-Associated X Proteinbcl-X ProteinBiomarkersCytochromes cHormones

Identifiers

PMID30431108
PMCPMC6257859
OpenAlexW2899957003

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.