Cited by 684Redox biology and oxidative stressNitric Oxide and Endothelin EffectsPancreatic function and diabetes

Diabetes associated cell stress and dysfunction: role of mitochondrial and non-mitochondrial ROS production and activity.

Open access
Newsholme, P., Haber, E. P., Hirabara, S. M., Rebelato, E. L. O., Procopio, J., Morgan, D., Oliveira‐Emilio, H. C., Carpinelli, A. R. +1 more·2007·The Journal of Physiology

Abstract

It is now widely accepted, given the current weight of experimental evidence, that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage caused by glucolipotoxicity in diabetes. The source of ROS in the insulin secreting pancreatic beta-cells and in the cells which are targets for insulin action has been considered to be the mitochondrial electron transport chain. While this source is undoubtably important, we provide additional information and evidence for NADPH oxidase-dependent generation of ROS both in pancreatic beta-cells and in insulin sensitive cells. While mitochondrial ROS generation may be important for regulation of mitochondrial uncoupling protein (UCP) activity and thus disruption of cellular energy metabolism, the NADPH oxidase associated ROS may alter parameters of signal transduction, insulin secretion, insulin action and cell proliferation or cell death. Thus NADPH oxidase may be a useful target for intervention strategies based on reversing the negative impact of glucolipotoxicity in diabetes.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1113/jphysiol.2007.135871

Cites

153 of 153 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Chronically increased ROS production can induce β-cell death and result in gradual onset of diabetes.

    “Chronically increased ROS production could also induce ␤-cell death and result in gradual onset of diabetes (249 -253).”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Newsholme, P., Haber, E. P., Hirabara, S. M., Rebelato, E. L. O., Procopio, J., Morgan, D., Oliveira‐Emilio, H. C., Carpinelli, A. R., & Curi, R.
Affiliations
  • University College Dublin (IE)
  • Hebrew University of Jerusalem (IL)
  • Universidade de São Paulo (BR)
  • Universidade Estadual de Ponta Grossa (BR)
Corresponding author
Newsholme, P.
Venue
The Journal of Physiology
Publisher
Wiley
Published
2007-08
Volume
583
Issue
1
Pages
9-24
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2164564813
Cited by
684
References
153
Citations by year
2026: 18 · 2025: 17 · 2024: 22 · 2023: 18 · 2022: 35 · 2021: 33 · 2020: 42 · 2019: 34 · 2018: 33 · 2017: 37 · 2016: 31 · 2015: 38 · 2014: 46 · 2013: 49 · 2012: 55
FWCI
3.27
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust
  • Health Research Board
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
diabetes mellitus, reactive oxygen species, NADPH oxidase, mitochondrial reactive oxygen species, glucolipotoxicity, pancreatic beta cells, insulin secretion, insulin action, mitochondrial uncoupling proteins, cellular energy metabolism, signal transduction, cell proliferation, cell death
MeSH terms
Animals, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Mitochondria, Apoptosis, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Insulin-Secreting Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review