Evidence map›Paper›PMID 40197538›Full record

ArticleThe Journal of cell biology2025

Rab GTPases are evolutionarily conserved signals mediating selective autophagy.

Pengwei Zhao, Rui Tian, Dandan Song, Qi Zhu, Xianming Ding, Jianqin Zhang, Beibei Cao, Mengyuan Zhang, Yilu Xu, Jie Fang and 6 more

Abstract read
In one paragraph

Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Rab12 is a regulator of mitophagy and mitochondrial homeostasis.bioRxiv : the preprint server for biology · 2026
    Article
  4. Rab14 promotes Parkin-mediated mitophagy.Molecular biology of the cell · 2025
    Article
  5. ER-driven Contact Sites in Autophagosome Biogenesis Sequence.Contact (Thousand Oaks (Ventura County, Calif.))
    Review
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

16 authors.

Pengwei Zhao *Center for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0006-4027-2547
Rui Tian *Center for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0000-1702-1121
Dandan Song *Center for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0002-5835-0620
Qi Zhu *Center for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0002-5493-8769
Xianming Ding *Center for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0000-0002-9256-2419
Jianqin ZhangCenter for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0002-2635-0300
Beibei CaoThe Fourth Affiliated Hospital, Zhejiang University School of Medicine , Yiwu, China.ORCID 0009-0006-0789-1282
Mengyuan ZhangCenter for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0000-7264-628X
Yilu XuCenter for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0009-0006-9413-8909
Jie FangInstitute of Translational Medicine, Zhejiang University , Hangzhou, China.ORCID 0009-0002-6377-4479
Jieqiong TanCenter for Medical Genetics, School of Life Sciences, Central South University , Changsha, China.ORCID 0000-0003-0730-1095
Cong YiDepartment of Biochemistry, and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6853-6563
Hongguang XiaDepartment of Biochemistry, and Department of Hepatobiliary and Pancreatic Surgery of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0003-3044-9282
Wei LiuCenter for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0000-0002-2046-6225
Wei ZouThe Fourth Affiliated Hospital, Zhejiang University School of Medicine , Yiwu, China.ORCID 0000-0003-4885-7313
Qiming SunCenter for Metabolism Research, the Fourth Affiliated Hospital of Zhejiang University School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University , Yiwu, China.ORCID 0000-0003-4988-9886

Funding

Ministry of Science and Technology of the People's Republic of China 2024YFA1803003National Natural Science Foundation of China 92254307
6 · The paper itself

Abstract

Selective autophagy plays a crucial role in maintaining cellular homeostasis by specifically targeting unwanted cargo labeled with "autophagy cues" signals for autophagic degradation. In this study, we identify Rab GTPases as a class of such autophagy cues signals involved in selective autophagy. Through biochemical and imaging screens, we reveal that human Rab GTPases are common autophagy substrates. Importantly, we confirm the conservation of Rab GTPase autophagic degradation in different model organisms. Rab GTPases translocate to damaged mitochondria, lipid droplets, and invading Salmonella-containing vacuoles (SCVs) to serve as degradation signals. Furthermore, they facilitate mitophagy, lipophagy, and xenophagy, respectively, by recruiting receptors. This interplay between Rab GTPases and receptors may ensure the de novo synthesis of isolation membranes around Rab-GTPase-labeled cargo, thereby mediating selective autophagy. These processes are further influenced by upstream regulators such as LRRK2, GDIs, and RabGGTase. In conclusion, this study unveils a conserved mechanism involving Rab GTPases as autophagy cues signals and proposes a model for the spatiotemporal control of selective autophagy.

Indexed as

AutophagyEvolution, Molecularrab GTP-Binding ProteinsSignal TransductionAnimalsHeLa CellsHumansMitochondriaMitophagyrab GTP-Binding Proteins

Identifiers

PMID40197538
PMCPMC11977514

What OpenQuestion holds

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Registered trials

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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.