Evidence map›Paper›PMID 35968729›Full record

ArticleAutophagy2023

Targeting mitophagy to promote apoptosis is a potential therapeutic strategy for cancer.

Yancheng Tang, Liming Wang, Jiangjiang Qin, Yingying Lu, Han-Ming Shen, Hu-Biao Chen

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.8field-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

24 citing papers in PubMed, 40 citations in OpenAlex.

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  10. MRG15 promotes cell apoptosis through inhibition of mitophagy in hyperlipidemic acute pancreatitis.Apoptosis : an international journal on programmed cell death · 2025
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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

6 authors at 6 institutions in 3 countries.

Yancheng TangSchool of Biomedical Science, Hunan University, Changsha, Hunan, China.
Liming WangSchool of Biomedical Science, Hunan University, Changsha, Hunan, China.
Jiangjiang QinThe Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
Yingying LuDepartment of Medical Research, Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China.
Han-Ming ShenFaculty of Health Sciences, University of Macau, Macau, China.
Hu-Biao ChenSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, SAR, China.
Hong Kong Baptist University · HKHunan University · CNThe Seventh Affiliated Hospital of Sun Yat-sen University · CNUniversity of Chinese Academy of Sciences · CNUniversity of Macau · MOZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many anticancer agents exert cytotoxicity and trigger apoptosis through the induction of mitochondrial dysfunction. Mitophagy, as a key mitochondrial quality control mechanism, can remove damaged mitochondria in an effective and timely manner, which may result in drug resistance. Although the implication of mitophagy in neurodegenerative diseases has been extensively studied, the role and mechanism of mitophagy in tumorigenesis and cancer therapy are largely unknown. In a recent study, we found that the inhibition of PINK1-PRKN-mediated mitophagy can significantly enhance the anticancer efficacy of magnolol, a natural product with potential anticancer properties. On the one hand, magnolol can induce severe mitochondrial dysfunction, including mitochondrial depolarization, excessive mitochondrial fragmentation and the generation of mitochondrial ROS, leading to apoptosis. On the other hand, magnolol induces PINK1-PRKN-dependent mitophagy via activation of two rounds of feedforward amplification loops. The blockage of mitophagy through genetic or pharmacological approaches promotes rather than attenuates magnolol-induced cell death. Furthermore, inhibition of mitophagy by using distinct inhibitors targeting different mitophagic stages effectively enhances magnolol's anticancer efficacy in vivo. Taken together, our findings strongly indicate that manipulation of mitophagy in cancer treatment will be a promising therapeutic strategy for overcoming cancer drug resistance and improving the therapeutic efficacy of anticancer agents.

Indexed as

Antineoplastic AgentsNeoplasmsApoptosisAutophagyBiphenyl CompoundsHumansLignansMitophagyProtein KinasesUbiquitin-Protein LigasesAntineoplastic AgentsBiphenyl CompoundsLignansmagnololProtein KinasesUbiquitin-Protein Ligases

Identifiers

PMID35968729
PMCPMC9980546
OpenAlexW4291209158

What OpenQuestion 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 OpenQuestion graph.