Evidence map›Paper›PMID 24606800›Full record

ReviewCurrent pharmaceutical design2014

Mitochondrial biogenesis: regulation by endogenous gases during inflammation and organ stress.

Hagir B Suliman, Claude A Piantadosi

Open access · bronzeAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
    Review
  3. Review
  4. The Dual Role of Exogenous Hydrogen Sulfide (HAntioxidants (Basel, Switzerland) · 2025
    Article
  5. Mitochondrial Dysfunction in Cardiovascular Diseases.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Curcumin and Heme Oxygenase: Neuroprotection and Beyond.International journal of molecular sciences · 2019
    Review
  16. Review
  17. Article
  18. A timeline of hydrogen sulfide (HBiochemical pharmacology · 2018
    Review
  19. Review
  20. Article
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.

Hagir B Suliman
Claude A PiantadosiDepartment of Medicine, Duke University Medical Center, 200 Trent Drive Durham, NC 27710 USA. Piant001@mc.duke.edu.
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
Redox Regulation of Lung Mitochondrial Biogenesis in Sepsis/PneumoniaR01AI095424 · NIAID · DUKE UNIVERSITY · PI PIANTADOSI, CLAUDE A · 2012 to 2016
$1.9M
Respiration in SepsisI01BX001926 · VA · DURHAM VA MEDICAL CENTER · PI PIANTADOSI, CLAUDE A · 2013 to 2016
–
BLRD VA I01 BX001926NHLBI NIH HHS P01 HL108801NHLBI NIH HHS P01-HL108801NIAID NIH HHS R01 AI095424
6 · The paper itself

Abstract

The influence of mitochondrial dysfunction on pathological states involving inflammatory and/or oxidative stress in tissues that do not show frank cellular apoptosis or necrosis has been rather difficult to unravel, and the literature is replete with contradictory information. Although such discrepancies have many potential causes related to the type of injurious agent, the severity and duration of the injury, and the particular cells and tissues and the functions involved, it is the successful induction of cellular adaptive responses that ultimately governs the resolution of mitochondrial dysfunction and survival of the cell. Much recent attention has been devoted to unraveling the signaling pathways that activate mitochondrial biogenesis and other processes involved in mitochondrial quality control (QC) during inflammatory and oxidative stress with an eye towards the development of novel targets for therapeutic mitigation of the resultant tissue damage. This review provides a brief overview of this emerging field with an emphasis on the role of signaling through the endogenous gases (NO, CO and H2S) and a redox-based approach that brings transparency to key factors that contribute to the resolution of mitochondrial dysfunction and the maintenance of cell vitality. We make the case that targeted stimulation of mitochondrial biogenesis could be a potentially valuable approach for the development of new therapies for the treatment of diseases for which mitochondrial damage is a major consideration.

Indexed as

AnimalsCarbon MonoxideCell SurvivalEnergy MetabolismHumansHydrogen SulfideInflammationMitochondriaMultiple Organ FailureNitric OxideOxidative StressReactive Oxygen SpeciesCarbon MonoxideHydrogen SulfideNitric OxideReactive Oxygen Species

Identifiers

PMID24606800
PMCPMC4276344
OpenAlexW2069429029

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.