Evidence map›Paper›PMID 23256813›Full record

ReviewFuture medicinal chemistry2013

Targeting cancer cell mitochondria as a therapeutic approach.

Shijun Wen, Daqian Zhu, Peng Huang

Open access · greenAbstract readReview
In one paragraph

Review in Future medicinal chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
2.7field-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

88 citing papers in PubMed, 201 citations in OpenAlex.

  1. Review
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28 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

3 authors at 2 institutions in 2 countries.

Shijun WenState Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Daqian Zhu
Peng Huang
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

Superoxide, ROS, and novel targets for cancer therapyR01CA085563 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2001 to 2016
$3.1M
p53 in Cellular Response to ROS-Mediated DNA DamageR01CA100428 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2003 to 2012
$2.7M
NCI NIH HHS CA085563NCI NIH HHS CA100428NCI NIH HHS R01 CA085563NCI NIH HHS R01 CA100428
6 · The paper itself

Abstract

Mitochondria are double membrane-enveloped organelles that play a central role in cellular metabolism, calcium homeostasis, redox signaling and cell fates. They function as main generators of ATP, metabolites for the construction of macromolecules and reactive oxygen species. In many cancer cells, mitochondria seem dysfunctional, manifested by a shift of energy metabolism from oxidative phosphorylation to active glycolysis and an increase in reactive oxygen species generation. These metabolic changes are often associated with upregulation of NAD(P)H oxidase. Importantly, the metabolic reprogramming in a cancer cell is mechanistically linked to oncogenic signals. Targeting mitochondria as a cancer therapeutic strategy has attracted much attention in the recent years and multiple review articles in this area have been published. This article attempts to provide an update on recent progress in identification of mitochondria-associated molecules as potential anticancer targets and the respective targeting compounds.

Indexed as

HomeostasisHumansMitochondriaNADPH OxidasesNeoplasmsOxidative PhosphorylationNADPH Oxidases

Identifiers

PMID23256813
PMCPMC3587793
OpenAlexW2048068073

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.