Evidence map›Paper›PMID 41596620›Full record

ArticleInternational journal of molecular sciences2026

Characterization of Large Extracellular Vesicles Released by Apoptotic and Pyroptotic Cells.

Delaram Khamari, Nora Fekete, Ririka Tamura, Raeeka Khamari, Agnes Kittel, Bence Nagy, Luigi Menna, Zsuzsanna Darula, Alicia Galinsoga, Eva Hunyadi-Gulyas and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Delaram KhamariInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-7162-0694
Nora FeketeInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0001-9721-765X
Ririka TamuraInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.
Raeeka KhamariHenri Warembourg Faculty of Medicine, Lille University Hospital (CHU), 59037 Lille, France.
Agnes KittelHUN-REN (Hungarian Research Network), Institute of Experimental Medicine, 1083 Budapest, Hungary.
Bence NagyInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.
Luigi MennaInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.
Zsuzsanna DarulaSingle Cell Omics Advanced Core Facility, Hungarian Centre of Excellence for Molecular Medicine, 6728 Szeged, Hungary.ORCID 0000-0003-1692-7591
Alicia GalinsogaInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.
Eva Hunyadi-GulyasProteomics Research Group, Core Facility, HUN-REN Biological Research Centre, 1083 Szeged, Hungary.ORCID 0000-0003-2089-1499
Maximilien BenczeU955-IMRB, Inserm, UPEC, ENVA, EFS, Team Relaix, Biology of the Neuromuscular System, 94000 Créteil, France.ORCID 0000-0002-3088-4818
Edit I BuzasInstitute of Genetics, Cell- and Immunobiology, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-3744-206X

Funding

EU Horizon 2020 No. 739593.EU Initial Training-ITN-FP7-PEOPLE-2011-ITNEU + Hungarian Government VEKOP-2.3.2-16-2016-00002, VEKOP-2.3.3-15-2017-00016EU+ Hungarian Government RRF-2.3.1-21-2022-00003EU + NKFIH 2019-2.1.7-ERA-NET-2021-00015Ministry of Culture and Innovation of Hungary from the National Research, Development and Innovation Fund 2022-2.1.1-NLNational Research, Development and Innovation Office NVKP_16-1-2016-0004National Research, Development and Innovation Office TKP2021-EGA-23NKFIH 150767 ADVANCED grantUniversity Paris Est Créteil Project no. 2022-2.1.1-NL-2022-00005
6 · The paper itself

Abstract

Extracellular vesicles (EVs) are emerging as key factors in maintaining cellular homeostasis, critical mediators of intercellular communication, potential biomarkers, and therapeutic tools. While small EVs have been extensively characterized, the molecular signatures of large EVs (including those generated during regulated cell death pathways) remain poorly defined. Here, we investigated the characteristics of large EVs released during apoptosis and pyroptosis by human monocytic cell lines (THP-1 and U937). Apoptosis was induced by staurosporine and blocked using the pan-caspase inhibitor Q-VD-OPh, whereas pyroptosis was triggered by LPS/nigericin and inhibited with a selective NLRP3 inhibitor. We found that both forms of regulated cell death markedly enhanced the release of large EVs. Both apoptotic and pyroptotic large EVs showed increased Annexin V binding and decreased CD9 expression compared with those released by healthy cells. Large EVs derived from apoptotic and pyroptotic cells exhibited distinct proteomic profiles. Pyroptotic large EVs carried interacting protein networks of RNA-binding proteins and chromatin-associated proteins many of which are known damage-associated molecular patterns or alarmins. In contrast, we found that a subpopulation of apoptotic large EVs was characterized by the presence of dsDNA, and active caspase-3/7. Together, our data shed light on the specific protein cargo of large EVs released by cells during apoptosis and pyroptosis. This study identifies candidate markers of large EVs released by dying cells and may enhance our understanding of the role of EVs in regulated cell death.

Indexed as

ApoptosisExtracellular VesiclesPyroptosisCaspase 3Caspase 7HumansProteomicsTHP-1 CellsU937 CellsCaspase 3Caspase 7apoptosiscell deathextracellular vesiclespyroptosis

Identifiers

PMID41596620
PMCPMC12841904

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.