Evidence map›Paper›PMID 34777681›Full record

ReviewOxidative medicine and cellular longevity2021

Interplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival.

Brittney Joy-Anne Foo, Jie Qing Eu, Jayshree L Hirpara, Shazib Pervaiz

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Brittney Joy-Anne FooDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore, Singapore.
Jie Qing EuDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore, Singapore.
Jayshree L HirparaCancer Science Institute, NUS, Singapore, Singapore.
Shazib PervaizDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore (NUS), Singapore, Singapore.ORCID https://orcid.org/0000-0002-4738-019X
National University of Singapore · SGNational University Cancer Institute, Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are the main powerhouse of the cell, generating ATP through the tricarboxylic acid cycle (TCA) and oxidative phosphorylation (OXPHOS), which drives myriad cellular processes. In addition to their role in maintaining bioenergetic homeostasis, changes in mitochondrial metabolism, permeability, and morphology are critical in cell fate decisions and determination. Notably, mitochondrial respiration coupled with the passage of electrons through the electron transport chain (ETC) set up a potential source of reactive oxygen species (ROS). While low to moderate increase in intracellular ROS serves as secondary messenger, an overwhelming increase as a result of either increased production and/or deficient antioxidant defenses is detrimental to biomolecules, cells, and tissues. Since ROS and mitochondria both regulate cell fate, attention has been drawn to their involvement in the various processes of carcinogenesis. To that end, the link between a prooxidant milieu and cell survival and proliferation as well as a switch to mitochondrial OXPHOS associated with recalcitrant cancers provide testimony for the remarkable metabolic plasticity as an important hallmark of cancers. In this review, the regulation of cell redox status by mitochondrial metabolism and its implications for cancer cell fate will be discussed followed by the significance of mitochondria-targeted therapies for cancer.

Indexed as

Energy MetabolismOxidative PhosphorylationAnimalsCell RespirationCell SurvivalHumansMitochondriaNeoplasmsOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID34777681
PMCPMC8580634
OpenAlexW3208967526

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.