Evidence map›Paper›PMID 40913644›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2026

A comprehensive insight into NETosis-extracellular vesicle crosstalk in autoimmune diseases.

Mohammed Hashim Mohammed, Sumaya Ayad Abdulrazzaq, Aysar Ashour Khalaf, Ashok Kumar Bishoyi, Roopashree R, Aditya Kashyap, Kamal Kant Joshi, Arshed Shakir Kadim, Muthena Kariem, Abed J Kadhim

Abstract readReview
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In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Mohammed Hashim MohammedMedical Laboratory Techniques Department, College of Health and Medical Technology, Al-Maarif University, Anbar, Iraq.
Sumaya Ayad AbdulrazzaqCenter of Desert Studies, University of Anbar, Anbar, Iraq. sumaya.ayad@uoanbar.edu.iq.
Aysar Ashour KhalafBiology Department, Faculty of Education for Pure Science, University of Kerbala, Kerbala, Iraq.
Ashok Kumar BishoyiMarwadi University Research Center, Department of Microbiology, Faculty of Science, Marwadi University, Rajkot, 360003, Gujarat, India.
Roopashree RDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bangalore, Karnataka, India.
Aditya KashyapCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Kamal Kant JoshiDepartment of Allied Science, Graphic Era Hill University, Dehradun, India.
Arshed Shakir KadimRadiological Techniques Department, College of Health and Medical Techniques, Al-Mustaqbal University, 51001, Babylon, Iraq.
Muthena KariemDepartment of Medical Analysis, Medical Laboratory Technique College, the Islamic University, Najaf, Iraq.
Abed J KadhimDepartment of Medical Engineering, Al-Nisour University College, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are granular and polymorphonuclear cells and one of the main participants of the innate immune system, which have received considerable attention due to the discovery of neutrophil extracellular traps (NETs). Extracellular vesicles (EVs), particularly those released by immune cells such as neutrophils, have been associated with the immunopathogenesis of autoimmune diseases. Besides, studies have reported a fundamental correlation between EVs and NETosis in autoimmune diseases. Neutrophil-generated NET-derived EVs contain various cargos, especially autoantigens that either promote inflammation or cause tissue damage, thereby triggering the initiation or progression. The NETs-EVs pathogenic correlation involved in the immunopathogenesis of autoimmune diseases could provide therapeutic opportunities through approaches such as blocking neutrophil-generated NET formation and inhibiting NET-derived EV secretion. Determining the underlying mechanism by which NETs-EVs correlation participates in autoimmune disease pathogenesis may lead to identifying novel and specific therapeutic approaches.

Indexed as

Autoimmune DiseasesExtracellular TrapsExtracellular VesiclesNeutrophilsAnimalsHumansAutoimmune diseasesEVsImmune systemNETosisNeutrophils

Identifiers

PMID40913644

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.