Evidence map›Paper›PMID 40377476›Full record

ArticleThe Journal of cell biology2025

Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair.

Justin Krish Williams, Jordan Matthew Ngo, Abinayaa Murugupandiyan, Dorothy E Croall, H Criss Hartzell, Randy Schekman

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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Sorcin couples Annexin A11 recruitment to ESCRT-III assembly for plasma membrane repair.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  3. Article
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  6. Calpain inhibition by calpeptin modulates adipocyte lipid metabolism and secretome-mediated inflammatory crosstalk with hepatocytes.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  7. Article
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  11. Article
  12. Review
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  14. Endosome transcriptomics reveal trafficking of Cajal bodies into multivesicular bodies.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. Review
  17. Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies.medRxiv : the preprint server for health sciences · 2025
    Article
  18. Revisiting the role of Annexins in membrane trafficking.Cellular and molecular life sciences : CMLS · 2025
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Justin Krish WilliamsDepartment of Molecular and Cell Biology, University of California, Berkeley, CA, USA.ORCID 0000-0002-9447-5554
Jordan Matthew NgoDepartment of Molecular and Cell Biology, University of California, Berkeley, CA, USA.ORCID 0000-0002-6566-3919
Abinayaa MurugupandiyanDepartment of Molecular and Cell Biology, University of California, Berkeley, CA, USA.ORCID 0009-0004-7639-7355
Dorothy E CroallDepartment of Biochemistry, Microbiology and Molecular Biology, University of Maine, Orono, ME, USA.ORCID 0000-0001-8214-8911
H Criss HartzellDepartment of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.ORCID 0000-0002-3393-1528
Randy SchekmanDepartment of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, CA, USA.ORCID 0000-0001-8615-6409

Funding

Howard Hughes Medical InstituteNIH HHS F31University of California, Berkeley
6 · The paper itself

Abstract

Microvesicles (MVs) are membrane-enclosed, plasma membrane-derived particles released by cells from all branches of life. MVs have utility as disease biomarkers and may participate in intercellular communication; however, physiological processes that induce their secretion are not known. Here, we isolate and characterize annexin-containing MVs and show that these vesicles are secreted in response to the calcium influx caused by membrane damage. The annexins in these vesicles are cleaved by calpains. After plasma membrane injury, cytoplasmic calcium-bound annexins are rapidly recruited to the plasma membrane and form a scab-like structure at the lesion. In a second phase, recruited annexins are cleaved by calpains-1/2, disabling membrane scabbing. Cleavage promotes annexin secretion within MVs. Our data support a new model of plasma membrane repair, where calpains relax annexin-membrane aggregates in the lesion repair scab, allowing secretion of damaged membrane and annexins as MVs. We anticipate that cells experiencing plasma membrane damage, including muscle and metastatic cancer cells, secrete these MVs at elevated levels.

Indexed as

AnnexinsCalpainCell-Derived MicroparticlesCell MembraneAnimalsCalciumHumansAnnexinsCalciumCalpain

Identifiers

PMID40377476
PMCPMC12083247

What OpenQuestion holds

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LicenceCC BY
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.