Evidence map›Paper›PMID 29207597›Full record

ArticleOncotarget2017

Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes.

Lingling Chen, Chunyan Liu, Jianfeng Gao, Zhiwen Xie, Lawrence W C Chan, Damien J Keating, Yibin Yang, Jiazhong Sun, Fuling Zhou, Yongchang Wei and 2 more

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

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
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  4. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  20. The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes.International journal of molecular sciences · 2021
    Review
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

12 authors at 6 institutions in 3 countries.

Lingling ChenABSL-3 Laboratory at the Center for Animal Experiment and Institute of Animal Model for Human Disease, Wuhan University School of Medicine, Wuhan, P. R. China.
Chunyan LiuABSL-3 Laboratory at the Center for Animal Experiment and Institute of Animal Model for Human Disease, Wuhan University School of Medicine, Wuhan, P. R. China.
Jianfeng GaoABSL-3 Laboratory at the Center for Animal Experiment and Institute of Animal Model for Human Disease, Wuhan University School of Medicine, Wuhan, P. R. China.
Zhiwen XieSchool of Bioscience and Technology , Weifang Medical University, Weifang Shandong, P.R. China.
Lawrence W C ChanDepartment of Health Technology and Informatics, Hong Kong Polytechnic University, Hong Kong, Hong Kong.
Damien J KeatingDepartment of Human Physiology and Centre for Neuroscience, Flinders University, Adelaide, South Australia, Australia.
Yibin YangDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China.
Jiazhong SunDepartment of Respiratory, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China.
Fuling ZhouDepartment of Hematology and Radiation, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China.
Yongchang WeiDepartment of Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China.
Xiuli MenSchool of Basic Medical Sciences, North China University of Science and Technology, Tangshan, P.R. China.
Sijun YangABSL-3 Laboratory at the Center for Animal Experiment and Institute of Animal Model for Human Disease, Wuhan University School of Medicine, Wuhan, P. R. China.
Wuhan University · CNFlinders University · AUHong Kong Polytechnic University · HKNorth China University of Science and Technology · CNWeifang Medical University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial function is essential to meet metabolic demand of pancreatic beta cells respond to high nutrient stress. Mitophagy is an essential component to normal pancreatic β-cell function and has been associated with β-cell failure in Type 2 diabetes (T2D). Our previous studies have indicated that mitochondrial Rho (Miro) GTPase-mediated mitochondrial dysfunction under high nutrient stress leads to NOD-like receptor 3 (NLRP3)-dependent proinflammatory responses and subsequent insulin resistance. However, the

Indexed as

diabetesHFDinsulin resistanceMiro1mitophagyPathology Section

Identifiers

PMID29207597
PMCPMC5710878
OpenAlexW2754677734

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.