Evidence map›Paper›PMID 25713188›Full record

ReviewDiabetes2015

Mitochondrial hormesis and diabetic complications.

Kumar Sharma

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
13.0field-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

116 citing papers in PubMed, 183 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
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  6. Article
  7. Review
  8. Article
  9. Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Article
  11. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Cardiomodulatory Effects of Cardiometabolic and Antihyperglycemic Medications: The Roles of Oxidative and Endoplasmic Reticulum Stress.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kumar SharmaCenter for Renal Translational Medicine, Division of Nephrology-Hypertension, Department of Medicine, University of California, San Diego, San Diego, CA, and Division of Nephrology-Hypertension, Veterans Affairs San Diego Healthcare System, Veterans Medical Research Foundation, San Diego, CA kumarsharma@ucsd.edu.
Veterans Medical Research Foundation of San Diego · US

Funding

Novel Paradigms in Diabetic ComplicationsDP3DK094352 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHARMA, KUMAR · 2011 to 2011
$6.0M
NIDDK NIH HHS DP3 DK094352NIDDK NIH HHS DP3-DK-094352
6 · The paper itself

Abstract

The concept that excess superoxide production from mitochondria is the driving, initial cellular response underlying diabetes complications has been held for the past decade. However, results of antioxidant-based trials have been largely negative. In the present review, the data supporting mitochondrial superoxide as a driving force for diabetic kidney, nerve, heart, and retinal complications are reexamined, and a new concept for diabetes complications--mitochondrial hormesis--is presented. In this view, production of mitochondrial superoxide can be an indicator of healthy mitochondria and physiologic oxidative phosphorylation. Recent data suggest that in response to excess glucose exposure or nutrient stress, there is a reduction of mitochondrial superoxide, oxidative phosphorylation, and mitochondrial ATP generation in several target tissues of diabetes complications. Persistent reduction of mitochondrial oxidative phosphorylation complex activity is associated with the release of oxidants from nonmitochondrial sources and release of proinflammatory and profibrotic cytokines, and a manifestation of organ dysfunction. Restoration of mitochondrial function and superoxide production via activation of AMPK has now been associated with improvement in markers of renal, cardiovascular, and neuronal dysfunction with diabetes. With this Perspective, approaches that stimulate AMPK and PGC1α via exercise, caloric restriction, and medications result in stimulation of mitochondrial oxidative phosphorylation activity, restore physiologic mitochondrial superoxide production, and promote organ healing.

Indexed as

AMP-Activated Protein KinasesAnimalsDiabetes ComplicationsHumansMitochondriaOxidative PhosphorylationOxidative StressReactive Oxygen SpeciesSuperoxidesAMP-Activated Protein KinasesReactive Oxygen SpeciesSuperoxides

Identifiers

PMID25713188
PMCPMC4338592
OpenAlexW2130176433

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.