Evidence map›Paper›PMID 38081963›Full record

ReviewOncogene2024

ROS production by mitochondria: function or dysfunction?

Flavio R Palma, Benjamin N Gantner, Marcelo J Sakiyama, Cezar Kayzuka, Sanjeev Shukla, Riccardo Lacchini, Brian Cunniff, Marcelo G Bonini

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed, 1 pooled it
59.7field-weighted citation impact, top 1% 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

246 citing papers in PubMed, 1 synthesis or guideline pooled it, 388 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. Article
  9. Oxygen-vacancy-engineered t-ZnO-CeOBioactive materials · 2026
    Article
  10. Lipidomic Remodeling by HILPDA in Granulosa Cells Impairs Ovarian Reserve Through Disruption of Mitochondrial and Endoplasmic Reticulum Homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  11. HPlant cell reports · 2026
    Article
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186 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

8 authors at 5 institutions in 3 countries.

Flavio R PalmaDepartment of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University, Chicago, IL, USA.ORCID 0000-0003-4350-2708
Benjamin N GantnerDepartment of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.ORCID 0000-0002-6947-7670
Marcelo J SakiyamaDepartment of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University, Chicago, IL, USA.
Cezar KayzukaDepartment of Pharmacology, Ribeirao Preto College of Nursing, University of Sao Paulo, Sao Paulo, Brazil.
Sanjeev ShuklaDepartment of Biological Sciences, Indian Institute of Science Education and Research Bhopal, Bhopal, India.ORCID 0000-0003-3361-0588
Riccardo LacchiniDepartment of Psychiatric Nursing and Human Sciences, Ribeirao Preto College of Nursing, University of Sao Paulo, Sao Paulo, Brazil.
Brian CunniffDepartment of Pathology and Laboratory Medicine, Larner School of Medicine, University of Vermont, Burlington, VT, USA.
Marcelo G BoniniDepartment of Medicine, Division of Hematology Oncology, Feinberg School of Medicine and the Robert H. Lurie Comprehensive Cancer Center of Chicago, Northwestern University, Chicago, IL, USA. Marcelo.bonini@northwestern.edu.ORCID 0000-0003-1193-1428
Northwestern University · USUniversidade de São Paulo · BRIndian Institute of Science Education and Research, Bhopal · INMedical College of Wisconsin · USUniversity of Vermont · US

Funding

A redox-sensitive switch in the macrophage nucleus regulates acute phaseinflammatory injuryR01HL163820 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G., GANTNER, BENJAMIN N. · 2022 to 2025
$2.3M
MNSOD ACETYLATION PROMOTES CANCER STEM CELL PHENOTYPES IN BREAST CANCERR01CA216882 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G. · 2018 to 2022
$1.9M
Environmental Arsenic in the Subtype Specification of Breast CancerR01ES028149 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G. · 2018 to 2022
$1.8M
Arsenic suppresses progesterone receptor signaling and promotes tamoxifen resistance and metastasis of ER+ breast cancerR56ES033398 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BONINI, MARCELO G. · 2022 to 2022
$150k
U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA216882U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL163820U.S. Department of Health & Human Services | NIH | National Institute of Environmental Health Sciences (NIEHS) R01ES028149U.S. Department of Health & Human Services | NIH | National Institute of Environmental Health Sciences (NIEHS) R56033398
6 · The paper itself

Abstract

In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.

Indexed as

MitochondriaOxidative StressAdenosine TriphosphateHumansReactive Oxygen SpeciesSignal TransductionAdenosine TriphosphateReactive Oxygen Species

Identifiers

PMID38081963
OpenAlexW4389549916

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.