Evidence map›Paper›PMID 25556935›Full record

ReviewAntioxidants & redox signaling2015

Regulation of mitochondrial biogenesis and its intersection with inflammatory responses.

Anne D Cherry, Claude A Piantadosi

Open access · hybridAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
9.2field-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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mitochondrial Imaging Detects Early Cardiac Changes Following Cancer Immunotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
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  15. Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

31 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.

Anne D Cherry1 Department of Anesthesiology, Duke University Medical Center , Durham, North Carolina.
Claude A Piantadosi
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
NHLBI NIH HHS P01 HL108801NHLBI NIH HHS P01 HL108801-04
6 · The paper itself

Abstract

significanceMitochondria play a vital role in cellular homeostasis and are susceptible to damage from inflammatory mediators released by the host defense. Cellular recovery depends, in part, on mitochondrial quality control programs, including mitochondrial biogenesis. RECENT ADVANCES: Early-phase inflammatory mediator proteins interact with PRRs to activate NF-κB-, MAPK-, and PKB/Akt-dependent pathways, resulting in increased expression or activity of coactivators and transcription factors (e.g., PGC-1α, NRF-1, NRF-2, and Nfe2l2) that regulate mitochondrial biogenesis. Inflammatory upregulation of NOS2-induced NO causes mitochondrial dysfunction, but NO is also a signaling molecule upregulating mitochondrial biogenesis via PGC-1α, participating in Nfe2l2-mediated antioxidant gene expression and modulating inflammation. NO and reactive oxygen species generated by the host inflammatory response induce the redox-sensitive HO-1/CO system, causing simultaneous induction of mitochondrial biogenesis and antioxidant gene expression. CRITICAL ISSUES: Recent evidence suggests that mitochondrial biogenesis and mitophagy are coupled through redox pathways; for instance, parkin, which regulates mitophagy in chronic inflammation, may also modulate mitochondrial biogenesis and is upregulated through NF-κB. Further research on parkin in acute inflammation is ongoing. This highlights certain common features of the host response to acute and chronic inflammation, but caution is warranted in extrapolating findings across inflammatory conditions. FUTURE DIRECTIONS: Inflammatory mitochondrial dysfunction and oxidative stress initiate further inflammatory responses through DAMP/PRR interactions and by inflammasome activation, stimulating mitophagy. A deeper understanding of mitochondrial quality control programs' impact on intracellular inflammatory signaling will improve our approach to the restoration of mitochondrial homeostasis in the resolution of acute inflammation.

Indexed as

Mitochondrial TurnoverSignal TransductionAnimalsCytokinesHumansInflammationMitochondriaMitophagyOxidation-ReductionOxidative StressTranscription FactorsCytokinesTranscription Factors

Identifiers

PMID25556935
PMCPMC4390030
OpenAlexW2005184671

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.