Evidence map›Paper›PMID 30312515›Full record

ReviewCancer science2018

Mitochondrial network structure homeostasis and cell death.

Long-Long Xie, Feng Shi, Zheqiong Tan, Yueshuo Li, Ann M Bode, Ya Cao

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
6.9field-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

100 citing papers in PubMed, 184 citations in OpenAlex.

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40 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

6 authors at 2 institutions in 4 countries.

Long-Long XieKey Laboratory of Cancer Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0001-7404-221X
Feng ShiKey Laboratory of Cancer Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Zheqiong TanKey Laboratory of Cancer Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Yueshuo LiKey Laboratory of Cancer Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Ann M BodeThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Ya CaoKey Laboratory of Cancer Carcinogenesis and Invasion, Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China.
Central South University · CNUniversity of Minnesota · US

Funding

College Students' Innovation Project of Central South University 2018zzts230College Students' Innovation Project of Central South University 2018zzts234Open-End Fund for the Valuable and Precision Instruments of Central South University CSUZC201744State Key Program of National Natural Science Foundation of China 81430064
6 · The paper itself

Abstract

Mitochondria are the major cellular energy-producing organelles and intracellular source of reactive oxygen species. These organelles are responsible for driving cell life and death through mitochondrial network structure homeostasis, which is determined by a balance of fission and fusion. Recent advances revealed that a number of components of the fission and fusion machinery, including dynamin-related protein 1 (Drp1), mitofusin1/2 (Mfn1/2) and Optic atrophy 1 (OPA1), that have been implicated in mitochondrial shape changes are indispensible for autophagy, apoptosis and necroptosis. Drp1 is the main regulator of mitochondrial fission and has become a key point of contention. The controversy focuses on whether Drp1 is directly involved in the regulation of cell death and, if involved, whether is it a stimulator or a negative regulator of cell death. Here, we examine the relevance of the homeostasis of the mitochondrial network structure in 3 different types of cell death, including autophagy, apoptosis and necroptosis. Furthermore, a variety of cancers often exhibit a fragmented mitochondrial phenotype. Thus, the fragmented ratio can reflect tumor progression that predicts prognosis and therapeutic response. In addition, we investigate whether the targeting of the mitochondrial fission protein Drp1 could be a novel therapeutic approach.

Indexed as

AnimalsCell DeathDynaminsGTP PhosphohydrolasesHomeostasisHumansMicrotubule-Associated ProteinsMitochondriaMitochondrial DynamicsMitochondrial Membrane Transport ProteinsMitochondrial ProteinsNeoplasmsPrognosisDNM1L protein, humanDynaminsGTP PhosphohydrolasesMfn1 protein, humanMicrotubule-Associated ProteinsMitochondrial Membrane Transport ProteinsMitochondrial ProteinsOPA1 protein, humancancerdynamin-related protein 1fissionfusionmitochondrial network structure homeostasis

Identifiers

PMID30312515
PMCPMC6272111
OpenAlexW2896563358

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.