Evidence map›Paper›PMID 22414059›Full record

ReviewCurrent diabetes reviews2012

The role of peroxidation of mitochondrial membrane phospholipids in pancreatic β -cell failure.

Zhongmin A Ma

Abstract readReview
In one paragraph

Review in Current diabetes reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Multi-Omics Analysis of a Spontaneous Type 2 Diabetes Model inInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Serotonin Influences Insulin Secretion in Rat Insulinoma INS-1E Cells.International journal of molecular sciences · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. International journal of molecular sciences · 2022
    Article
  11. Article
  12. Review
  13. Phospholipase iPLA2β acts as a guardian against ferroptosis.Cancer communications (London, England) · 2021
    Article
  14. Nutrients · 2021
    Article
  15. Article
  16. Review
  17. Review
  18. α-Cyperone Attenuates HFrontiers in pharmacology · 2020
    Article
  19. Article
  20. iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    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

1 author at 1 institution in 1 country.

Zhongmin A MaDivision of Experimental Diabetes and Aging, Department of Geriatrics and Palliative Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. Zhongmin.ma@mssm.edu
Icahn School of Medicine at Mount Sinai · US

Funding

YOGA LIFESTYLE INTERVENTION REDUCES BLOOD PRESSURE IN HIV-INFECTED ADULTSP41RR000954 · NCRR · WASHINGTON UNIVERSITY · PI TAYLOR, JOHN-STEPHEN ADOLFINO · 1985 to 2011
$16.0M
Mechanisms of neurodegeneration and brain iron accumulationR01NS063962 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MA, ZHONGMIN ALEX · 2009 to 2010
$763k
NCRR NIH HHS P41 RR000954NINDS NIH HHS R01 NS063962NINDS NIH HHS R01-NS063962
6 · The paper itself

Abstract

Type 2 diabetes (T2D) is characterized by peripheral insulin resistance and pancreatic islet β-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor to β-cell failure in the pathogenesis of T2D. This review focuses on mechanisms whereby reactive oxygen species (ROS) produced by β-cell in response to metabolic stress affect mitochondrial structure and function and lead to β-cell failure. Specifically, ROS oxidize mitochondrial membrane phospholipids such as cardiolipin, which impairs membrane integrity and leads to cytochrome c release and apoptosis. In addition, ROS activate UCP2 via peroxidation of the mitochondrial membrane phospholipids, which results in proton leak leading to reduced ATP synthesis and content in β-cells - critical parameters in the regulation of glucose-stimulated insulin secretion. Group VIA Phospholipase A2 (iPLA2β) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA2β-deficiency increases β-cell mitochondrial susceptibility to injury from ROS and predisposes to development of T2D. Interventions that attenuate the adverse effects of ROS on β-cell mitochondrial phospholipids may prevent or retard the development of T2D.

Indexed as

Diabetes Mellitus, Type 2FemaleHumansInsulinInsulin-Secreting CellsInsulin SecretionLipid PeroxidationMaleMitochondrial MembranesPhospholipidsReactive Oxygen SpeciesInsulinPhospholipidsReactive Oxygen Species

Identifiers

PMID22414059
PMCPMC4884441
OpenAlexW2316865662

What OpenQuestion holds

Textmetadata
LicenceTDM
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.