Evidence map›Paper›PMID 19650713›Full record

ReviewAntioxidants & redox signaling2010

Mitochondrial dysfunction in diabetes: from molecular mechanisms to functional significance and therapeutic opportunities.

William I Sivitz, Mark A Yorek

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 373 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
373citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

373 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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313 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

2 authors.

William I SivitzDepartment of Internal Medicine, Division of Endocrinology and Metabolism, Iowa City Veterans Affairs Medical Center and University of Iowa, Iowa City, Iowa, USA. william-sivitz@uiowa.edu
Mark A Yorek

Funding

SITE SPECIFIC ANTIINSULIN RECEPTOR ANTIBODIESP30DK025295 · NIDDK · UNIVERSITY OF IOWA · PI YOREK, MARK ANTHONY · 1986 to 2002
$2.6M
Prevention of Diabetic Neuropathy with ACE InhibitorsR01DK073990 · NIDDK · UNIVERSITY OF IOWA · PI YOREK, MARK A. · 2008 to 2012
$1.3M
Prevention of Diabetic Neuropathy with ACE InhibitorsR56DK073990 · NIDDK · UNIVERSITY OF IOWA · PI YOREK, MARK ANTHONY · 2006 to 2007
$497k
NIDDK NIH HHS DK073990NIDDK NIH HHS DK25295NIDDK NIH HHS R01 DK073990
6 · The paper itself

Abstract

Given their essential function in aerobic metabolism, mitochondria are intuitively of interest in regard to the pathophysiology of diabetes. Qualitative, quantitative, and functional perturbations in mitochondria have been identified and affect the cause and complications of diabetes. Moreover, as a consequence of fuel oxidation, mitochondria generate considerable reactive oxygen species (ROS). Evidence is accumulating that these radicals per se are important in the pathophysiology of diabetes and its complications. In this review, we first present basic concepts underlying mitochondrial physiology. We then address mitochondrial function and ROS as related to diabetes. We consider different forms of diabetes and address both insulin secretion and insulin sensitivity. We also address the role of mitochondrial uncoupling and coenzyme Q. Finally, we address the potential for targeting mitochondria in the therapy of diabetes.

Indexed as

AnimalsBlood GlucoseCell RespirationDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Electron TransportHumansInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionMembrane Potential, MitochondrialMiceMitochondriaMitochondrial DiseasesOxidative StressBlood GlucoseInsulinReactive Oxygen SpeciesSuperoxidesUbiquinone

Identifiers

PMID19650713
PMCPMC2824521

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.