Evidence map›Paper›PMID 29321664›Full record

ArticleOncogene2018

Mitochondrial fission and mitophagy depend on cofilin-mediated actin depolymerization activity at the mitochondrial fission site.

Guo-Bing Li, Hong-Wei Zhang, Ruo-Qiu Fu, Xiao-Ye Hu, Lei Liu, Yu-Nong Li, Yan-Xia Liu, Xin Liu, Jin-Jiao Hu, Qin Deng and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  6. Review
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  13. Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Article
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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

13 authors at 1 institution in 1 country.

Guo-Bing LiCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Hong-Wei ZhangCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Ruo-Qiu FuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Xiao-Ye HuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Lei LiuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Yu-Nong LiCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Yan-Xia LiuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Xin LiuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Jin-Jiao HuCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Qin DengCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Qing-Song LuoCollege of Pharmacy, Third Military Medical University, Chongqing, China.
Rong ZhangDepartment of Pharmacy, The Second Affiliated Hospital of Third Military Medical University, Chongqing, China. xqpharmacylab@126.com.
Ning GaoCollege of Pharmacy, Third Military Medical University, Chongqing, China. gaoning59@163.com.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria fission and mitophagy are fundamentally crucial to cellular physiology and play important roles in cancer progression. Developing a comprehensive understanding of the molecular mechanism underlying mitochondrial fission and mitophagy will provide novel strategies for cancer prevention and treatment. Actin has been shown to participate in mitochondrial fission and mitophagy regulation. Cofilin is best known as an actin-depolymerizing factor. However, the molecular mechanism by which cofilin regulates mitochondrial fission and mitophagy remains largely unknown. Here we report that knockdown of cofilin attenuates and overexpression of cofilin potentiates mitochondrial fission as well as PINK1/PARK2-dependent mitophagy induced by staurosporine (STS), etoposide (ETO), and carbonyl cyanide 3-chlorophenylhydrazone (CCCP). Cofilin-mediated-PINK1 (PTEN-induced putative kinase 1) accumulation mainly depends on its regulation of mitochondrial proteases, including peptidase mitochondrial processing beta (MPPβ), presenilin-associated rhomboid-like protease (PARL), and ATPase family gene 3-like 2 (AFG3L2), via mitochondrial membrane potential activity. We also found that the interaction and colocalization of G-actin/F-actin with cofilin at mitochondrial fission sites undergo constriction after CCCP treatment. Pretreatment with the actin polymerization inhibitor latrunculin B (LatB) increased and actin-depolymerization inhibitor jasplakinolide (Jas) decreased mitochondrial translocation of actin induced by STS, ETO, and CCCP. Both LatB and Jas abrogated CCCP-mediated mitochondrial fission and mitophagy. Our data suggest that G-actin is the actin form that is translocated to mitochondria, and the actin-depolymerization activity regulated by cofilin at the mitochondrial fission site is crucial for inducing mitochondrial fission and mitophagy.

Indexed as

Actin Depolymerizing FactorsActinsBinding SitesCells, CulturedHumansMitochondrial DynamicsMitophagyProtein KinasesProtein MultimerizationProtein TransportPTEN-Induced Putative KinaseUbiquitin-Protein LigasesActin Depolymerizing FactorsActinsparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligases

Identifiers

PMID29321664
OpenAlexW2784192559

What Socratic 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 Socratic graph.