Evidence map›Paper›PMID 40885798›Full record

ArticleNature communications2025

Evidence that mitochondria in macrophages are destroyed by microautophagy.

Shiou-Ling Lu, Siyu Chen, Kazuya Noda, Yangjie Li, Chao-Yuan Tsai, Hiroko Omori, Yumiko Kato, Zidi Zhang, Bohan Chen, Kanako Tokuda and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Development of AuACS applied materials & interfaces · 2026
    Article
  12. Article
  13. Review
  14. Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025
    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

19 authors.

Shiou-Ling Lu *Department of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0003-4308-1536
Siyu Chen *Department of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Kazuya Noda *Department of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Yangjie LiDepartment of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Chao-Yuan TsaiLaboratory of Immune Regulation, Immunology Frontier Research Center, The University of Osaka, Osaka, Japan.
Hiroko OmoriResearch Institute for Microbial Diseases (RIMD), The University of Osaka, Osaka, Japan.
Yumiko KatoDepartment of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Zidi ZhangDepartment of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Bohan ChenGraduate School of Frontier Biosciences, The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0009-0003-7753-4422
Kanako TokudaGraduate School of Frontier Biosciences, The University of Osaka, Osaka, Japan.
Tongxin ZhengDepartment of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Masahiro WakitaResearch Institute for Microbial Diseases (RIMD), The University of Osaka, Osaka, Japan.
Eiji HaraResearch Institute for Microbial Diseases (RIMD), The University of Osaka, Osaka, Japan.ORCID http://orcid.org/0000-0001-7821-3960
Mitsunori FukudaDepartment of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.ORCID http://orcid.org/0000-0002-8620-5853
Yoh WadaDepartment of Biological Sciences, Institute of Scientific and Industrial Research, The University of Osaka, Osaka, Japan.
Eiji MoritaDepartment of Biochemistry and Molecular Biology, Faculty of Agriculture and Life Science, Hirosaki University, Hirosaki, Japan.
Narikazu UzawaDepartment of Oral & Maxillofacial Oncology and Surgery, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Shinya MurakamiDepartment of Periodontology and Regenerative Dentistry, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Takeshi NodaDepartment of Oral Cellular Biology, Center for Frontier Oral Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan. noda.takeshi.dent@osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-3581-7961

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 20H05326MEXT | Japan Society for the Promotion of Science (JSPS) 20K15789MEXT | Japan Society for the Promotion of Science (JSPS) 22H04647MEXT | Japan Society for the Promotion of Science (JSPS) 23H02475MEXT | Japan Society for the Promotion of Science (JSPS) 25K09629
6 · The paper itself

Abstract

Microautophagy is an intracellular degradation process in which degradatory organelles, such as the lysosome, directly take up substrates by invagination and/or protrusion of their membranes. Here, we provide evidence that Rab32-positive, lysosome-related organelles in macrophages incorporate various other organelles, including endosomes and mitochondria. Our data indicates that, upon exposure to a mitochondria-damaging reagent, mitochondria can be directly engulfed by the lysosome-like organelles independently of macroautophagy or ESCRT machinery. Rab32 GTPase, phosphatidylinositol 3,5-bisphosphates, ubiquitination, and p62/SQSTM1 are crucial for this degradation. Furthermore, the degree of M1 polarization of macrophages, which is facilitated by metabolic reprogramming into increased glycolysis via mitochondrial elimination, is significantly reduced in Rab32/38 double-knockout macrophages. Thus, microautophagy plays a role in the physiological regulation of macrophages.

Indexed as

AutophagyMacrophagesMicroautophagyMitochondriaAnimalsEndosomesHumansLysosomesMiceMice, Inbred C57BLMice, Knockoutrab GTP-Binding ProteinsRAW 264.7 CellsSequestosome-1 ProteinUbiquitinationrab GTP-Binding ProteinsSequestosome-1 ProteinSqstm1 protein, mouse

Identifiers

PMID40885798
PMCPMC12398504

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.