Evidence map›Paper›PMID 30132505›Full record

ArticleInternational journal of molecular medicine2018

Opening of mitoKATP improves cardiac function and inhibits apoptosis via the AKT-Foxo1 signaling pathway in diabetic cardiomyopathy.

Peng Duan, Jinxin Wang, Yang Li, Shiqiang Wei, Feng Su, Sanlin Zhang, Yuhui Duan, Lin Wang, Qinglei Zhu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Forkhead box O1 transcription factor; a therapeutic target for diabetic cardiomyopathy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
  3. Review
  4. Article
  5. The Role of Forkhead Box O in Pathogenesis and Therapy of Diabetes Mellitus.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Mitochondrial Metal Ion Transport in Cell Metabolism and Disease.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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

9 authors at 2 institutions in 1 country.

Peng DuanDepartment of Cardiology, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Jinxin WangDepartment of Cardiology, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Yang LiDepartment of Cardiology, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Shiqiang WeiDepartment of Cardiology, Chinese PLA No. 371 Hospital, Xinxiang, Henan 453000, P.R. China.
Feng SuDepartment of Medical Administration, Chinese PLA No. 371 Hospital, Xinxiang, Henan 453000, P.R. China.
Sanlin ZhangDepartment of Cardiology, Chinese PLA No. 371 Hospital, Xinxiang, Henan 453000, P.R. China.
Yuhui DuanDepartment of Cardiology, Chinese PLA No. 371 Hospital, Xinxiang, Henan 453000, P.R. China.
Lin WangDepartment of Cardiology, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Qinglei ZhuDepartment of Cardiology, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Chinese PLA General Hospital · CNXinxiang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decreasing phosphorylation of AKT‑Foxo1 is closely associated with the onset of insulin resistance and apoptosis during diabetic cardiomyopathy (DCM). Opening of mitochondrial ATP‑sensitive potassium channels (mitoKATP) increases the expression of p‑AKT in the process of reperfusion injury. It was therefore hypothesized that opening of mitoKATP may regulate the AKT‑Foxo1 signaling pathway and improve cardiac function in DCM. In the present study, opening of mitoKATP by diazoxide (DZX) was found to improve cardiac function and attenuate cardiomyocyte apoptosis in db/db mice. DZX also significantly increased the expression of p‑AKT and p‑Foxo1. Similarly, DZX decreased the expression of the heart failure marker NT‑proBNP, increased mitochondrial membrane potential, inhibited apoptosis, and increased the expression of p‑AKT and p‑Foxo1 when mimicking insulin resistance in cultured cardiomyocytes. Moreover, the protective effects of DZX were completely blocked by the specific AKT inhibitor MK‑2206. These data suggest that the regulation of the AKT‑Foxo1 signaling pathway by mitoKATP plays an important role in improving cardiac function and inhibiting apoptosis in DCM, and may therefore be a new potential therapeutic target for DCM.

Indexed as

AnimalsApoptosisBlood GlucoseCaspase 3Diabetic CardiomyopathiesEchocardiographyForkhead Box Protein O1In Situ Nick-End LabelingMaleMembrane Potential, MitochondrialMiceNatriuretic Peptide, BrainPeptide FragmentsPotassium ChannelsProto-Oncogene Proteins c-aktRatsBlood GlucoseCaspase 3Forkhead Box Protein O1Foxo1 protein, mousemitochondrial K(ATP) channelNatriuretic Peptide, BrainPeptide FragmentsPotassium Channelspro-brain natriuretic peptide (1-76)Proto-Oncogene Proteins c-akt

Identifiers

PMID30132505
PMCPMC6192784
OpenAlexW2888638294

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.