Evidence map›Paper›PMID 26276086›Full record

ReviewPharmacological research2015

Mitochondrial ROS and cancer drug resistance: Implications for therapy.

Imoh S Okon, Ming-Hui Zou

Abstract readReview
In one paragraph

Review in Pharmacological research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 203 citations in OpenAlex.

  1. Article
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  10. Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025
    Review
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39 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.

Imoh S OkonCenter for Molecular and Translational Medicine, Georgia State University, Atlanta, GA 30303 USA. Electronic address: iokon@gsu.edu.
Ming-Hui ZouCenter for Molecular and Translational Medicine, Georgia State University, Atlanta, GA 30303 USA.
Georgia State University · US

Funding

Reactive Nitrogen species and Diabetic Endothelial DysfunctionR01HL079584 · NHLBI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ZOU, MING-HUI · 2004 to 2021
$7.3M
Inflammasome and unstable atherosclerotic plaquesR01HL089920 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2008 to 2022
$6.9M
AMP-Activated Protein Kinase in DiabetesR01HL080499 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2006 to 2019
$5.8M
Controlling VSMC Proliferation and MigrationR01HL110488 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2011 to 2020
$3.9M
Oxidant stress and diabetic endothelial dysfunctionR01HL074399 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2005 to 2013
$3.2M
Autophagy and VSMC migrationR01HL132500 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2016 to 2019
$2.7M
Suppression of Autophagy-Dependent Clearance Mitochondria in Type 2 DiabetesR01HL128014 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2015 to 2018
$2.4M
Prevention of High Fat Diet-Induced Vascular InjuryR01HL105157 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2010 to 2014
$1.8M
Angiotensin-II, GTPCH1 and 26S ProtesomesR01HL096032 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2009 to 2013
$1.8M
Sirt1, Vascular Aging, and Aortic AneurysmR01AG047776 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2014 to 2018
$1.5M
NHLBI NIH HHS R01 HL074399NHLBI NIH HHS R01 HL079584NHLBI NIH HHS R01 HL080499NHLBI NIH HHS R01 HL089920NHLBI NIH HHS R01 HL096032NHLBI NIH HHS R01 HL105157NHLBI NIH HHS R01 HL110488NHLBI NIH HHS R01 HL128014NHLBI NIH HHS R01 HL132500NIA NIH HHS R01 AG047776
6 · The paper itself

Abstract

Under physiological conditions, a well-coordinated and balanced redox system exists to ensure that reactive oxygen species (ROS) are appropriately utilized to accomplish specific functions, such as signaling and protein regulation. The influence of ROS within malignant cells, whether for good or bad may depend on several factors, such as tumor and tissue type, disease stage, treatment strategy, as well as duration, specificity and levels of ROS. What then are the known roles of ROS in cancer? Firstly, ROS significantly impacts cancer phenotypes. Secondly, the oxidative ROS property responsible for killing cancer cells, also impact secondary signaling networks. Thirdly, a strong correlation exist between ROS and genetic instability which may promote mutations. Finally, emerging observations suggest a role for mitochondrial ROS in cancer drug resistance, with implications for therapy. The mitochondria is a key regulator of metabolic-redox (meta-redox) alterations within cancer cells. Like a double-edged sword, mitochondrial ROS perturbations in cancer therapy may be beneficial or detrimental. However, harnessing ROS-specific cancer-targeting benefits remain a major challenge.

Indexed as

Drug Resistance, NeoplasmHumansMitochondriaNeoplasmsOxidation-ReductionOxidative StressReactive Oxygen SpeciesSignal TransductionReactive Oxygen SpeciesCancer drug resistanceMetabolic alterationsMitochondrial ROSOxidative stress

Identifiers

PMID26276086
PMCPMC4893310
OpenAlexW1458147944

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.