Evidence map›Paper›PMID 30601700›Full record

ReviewAmerican journal of physiology. Endocrinology and metabolism2019

Mitochondrial dysfunction in type 2 diabetes mellitus: an organ-based analysis.

Mark V Pinti, Garrett K Fink, Quincy A Hathaway, Andrya J Durr, Amina Kunovac, John M Hollander

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Endocrinology and metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 4 pooled it
14.6field-weighted citation impact, top 1% 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

234 citing papers in PubMed, 4 syntheses or guidelines pooled it, 412 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Pooled it
  5. Trial
  6. Trial
  7. Diabetes-Associated Cognitive Impairment: Pathophysiology and Emerging Therapies.Annals of clinical and translational neurology · 2026
    Review
  8. Review
  9. Article
  10. Review
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  13. Integrative Clinical and Functional Characterization of theDiagnostics (Basel, Switzerland) · 2026
    Article
  14. Article
  15. Review
  16. Article
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  19. Article
  20. Review

174 more citing papers are in PubMed but not listed here.

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.

Mark V PintiDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
Garrett K FinkDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
Quincy A HathawayDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
Andrya J DurrDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
Amina KunovacDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
John M HollanderDivision of Exercise Physiology, West Virginia University School of Medicine , Morgantown, West Virginia.
West Virginia University · US

Funding

miRNA Regulation of the Mitochondrial GenomeR01HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2017 to 2019
$1.3M
miRNA Regulation of the Mitochondrial GenomeR56HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2015 to 2015
$410k
NHLBI NIH HHS R01 HL128485NHLBI NIH HHS R56 HL128485
6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a systemic disease characterized by hyperglycemia, hyperlipidemia, and organismic insulin resistance. This pathological shift in both circulating fuel levels and energy substrate utilization by central and peripheral tissues contributes to mitochondrial dysfunction across organ systems. The mitochondrion lies at the intersection of critical cellular pathways such as energy substrate metabolism, reactive oxygen species (ROS) generation, and apoptosis. It is the disequilibrium of these processes in T2DM that results in downstream deficits in vital functions, including hepatocyte metabolism, cardiac output, skeletal muscle contraction, β-cell insulin production, and neuronal health. Although mitochondria are known to be susceptible to a variety of genetic and environmental insults, the accumulation of mitochondrial DNA (mtDNA) mutations and mtDNA copy number depletion is helping to explain the prevalence of mitochondrial-related diseases such as T2DM. Recent work has uncovered novel mitochondrial biology implicated in disease progressions such as mtDNA heteroplasmy, noncoding RNA (ncRNA), epigenetic modification of the mitochondrial genome, and epitranscriptomic regulation of the mtDNA-encoded mitochondrial transcriptome. The goal of this review is to highlight mitochondrial dysfunction observed throughout major organ systems in the context of T2DM and to present new ideas for future research directions based on novel experimental and technological innovations in mitochondrial biology. Finally, the field of mitochondria-targeted therapeutics is discussed, with an emphasis on novel therapeutic strategies to restore mitochondrial homeostasis in the setting of T2DM.

Indexed as

Adipose TissueBrainDiabetes Mellitus, Type 2DNA, MitochondrialEndothelium, VascularEpigenesis, GeneticExerciseHumansInsulin-Secreting CellsLiverMitochondriaMitochondria, HeartMitochondria, LiverMitochondria, MuscleMuscle, SkeletalMyocardiumDNA, Mitochondrialdiabetes mellitusmitochondria dysfunction

Identifiers

PMID30601700
PMCPMC6397358
OpenAlexW2908459563

What OpenQuestion holds

Textmetadata
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.