Evidence map›Paper›PMID 26377343›Full record

ReviewThe Journal of physiology2016

Mitochondria and carbon monoxide: cytoprotection and control of cell metabolism - a role for Ca(2+) ?

Sara R Oliveira, Cláudia S F Queiroga, Helena L A Vieira

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. 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
1.1field-weighted citation impact, top 24% 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, 55 citations in OpenAlex.

  1. Gas entrapping materials for damage control.Advanced drug delivery reviews · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Carbon Monoxide-Releasing Activity of Plant Flavonoids.Journal of agricultural and food chemistry · 2025
    Article
  6. Article
  7. Review
  8. Carbon monoxide licensing of MSCs enhances their efficacy through autophagy-mediated miRNA mechanisms.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Bioactivity of Inhaled Methane and Interactions With Other Biological Gases.Frontiers in cell and developmental biology · 2021
    Review
  16. Review
  17. Article
  18. Observational
  19. Article
  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

3 authors at 2 institutions in 1 country.

Sara R OliveiraCEDOC, NOVA Medical School, Universidade Nova de Lisboa, 1169-056, Lisboa, Portugal.
Cláudia S F QueirogaCEDOC, NOVA Medical School, Universidade Nova de Lisboa, 1169-056, Lisboa, Portugal.
Helena L A VieiraCEDOC, NOVA Medical School, Universidade Nova de Lisboa, 1169-056, Lisboa, Portugal.
Universidade Nova de Lisboa · PTUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbon monoxide (CO) is an endogenously produced gasotransmitter with important biological functions: anti-inflammation, anti-apoptosis, vasomodulation and cell metabolism modulation. The most recognized cellular target for CO is the mitochondria. Physiological concentrations of CO generate mitochondrial reactive oxygen species (ROS), which are signalling molecules for CO-induced pathways. Indeed, small amounts of ROS promote cytoprotection by a preconditioning effect. Furthermore, CO prevents cell death by limiting mitochondrial membrane permeabilization, which inhibits the release of pro-apoptotic factors into the cytosol; both events are ROS dependent. CO also increases the ability of mitochondria to take up Ca(2+) . Mitochondrial metabolism is modulated by CO, namely by increasing TCA cycle rate, oxidative phosphorylation and mitochondrial biogenesis, which, in turn, increases ATP production. CO's modulation of metabolism might be important for cellular response to diseases, namely cancer and ischaemic diseases. Finally, another cytoprotective role of CO involves the control of Ca(2+) channels. By limiting the activity of T-type and L-type Ca(2+) channels, CO prevents excitotoxicity-induced cell death and modulates cell proliferation. Several questions concerning Ca(2+) signalling, mitochondria and CO can be asked, for instance whether CO modulation of cell metabolism would be dependent on the mitochondrial Ca(2+) uptake capacity, since small amounts of Ca(2+) can increase mitochondrial metabolism. Whether CO controls Ca(2+) communication between mitochondria and endoplasmic reticulum is another open field of research. In summary, CO emerges as a key gasotransmitter in the control of several cellular functions of mitochondria: metabolism, cell death and Ca(2+) signalling.

Indexed as

AnimalsCalciumCalcium ChannelsCarbon MonoxideCell DeathCytoprotectionHumansMitochondriaReactive Oxygen SpeciesCalciumCalcium ChannelsCarbon MonoxideReactive Oxygen Species

Identifiers

PMID26377343
PMCPMC4967755
OpenAlexW1956141992

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.