Evidence map›Paper›PMID 23000245›Full record

ReviewFree radical biology & medicine2012

Redox regulation of mitochondrial biogenesis.

Claude A Piantadosi, Hagir B Suliman

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 180 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Recent advances in the role of gasotransmitters in necroptosis.Apoptosis : an international journal on programmed cell death · 2025
    Review
  15. Review
  16. Article
  17. A Feasibility Study of [Molecular imaging and biology · 2024
    Article
  18. Review
  19. Article
  20. Review

47 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 at 1 institution in 1 country.

Claude A PiantadosiDepartment of Medicine, Duke University Medical Center and the Durham VA Medical Center, Durham, NC 27710, USA. piant001@mc.duke.edu
Hagir B Suliman
Duke Medical Center · US

Funding

Mesenchymal Stromal Cell Conditioning by Carbon MonoxideP01HL108801 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHOI, AUGUSTINE M · 2011 to 2015
$13.8M
Regulation of mitochondrial biogenesis by heme oxygenase-1R01HL090679 · NHLBI · DUKE UNIVERSITY · PI PIANTADOSI, CLAUDE A · 2008 to 2011
$1.6M
Mitochondrial biogenesis in sepsis-induced organ dysfunctionR01GM084116 · NIGMS · DUKE UNIVERSITY · PI PIANTADOSI, CLAUDE A, WELTY-WOLF, KAREN E · 2009 to 2012
$1.3M
NHLBI NIH HHS HL090679NHLBI NIH HHS P01 HL108801NHLBI NIH HHS R01 HL090679NIGMS NIH HHS GM084116NIGMS NIH HHS R01 GM084116
6 · The paper itself

Abstract

The cell renews, adapts, or expands its mitochondrial population during episodes of cell damage or periods of intensified energy demand by the induction of mitochondrial biogenesis. This bigenomic program is modulated by redox-sensitive signals that respond to physiological nitric oxide (NO), carbon monoxide (CO), and mitochondrial reactive oxygen species production. This review summarizes our current ideas about the pathways involved in the activation of mitochondrial biogenesis by the physiological gases leading to changes in the redox milieu of the cell, with an emphasis on the responses to oxidative stress and inflammation. The cell's energy supply is protected from conditions that damage mitochondria by an inducible transcriptional program of mitochondrial biogenesis that operates in large part through redox signals involving the nitric oxide synthase and the heme oxygenase-1/CO systems. These redox events stimulate the coordinated activities of several multifunctional transcription factors and coactivators also involved in the elimination of defective mitochondria and the expression of counterinflammatory and antioxidant genes, such as IL10 and SOD2, as part of a unified damage-control network. The redox-regulated mechanisms of mitochondrial biogenesis schematically outlined in the graphical abstract link mitochondrial quality control to an enhanced capacity to support the cell's metabolic needs while improving its resistance to metabolic failure and avoidance of cell death during periods of oxidative stress.

Indexed as

Mitochondrial TurnoverAnimalsEnergy MetabolismGene Expression RegulationHeme Oxygenase-1HomeostasisHumansNitric OxideOxidation-ReductionOxidative StressHeme Oxygenase-1Nitric Oxide

Identifiers

PMID23000245
PMCPMC3604744
OpenAlexW2030591331

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.