Evidence map›Paper›PMID 42757451›Full record

ReviewBiochemical Society transactions2026

NINJ1: implications for plasma membrane rupture and disease.

Elliott M Bernard, Ella Hartenian

Abstract readReview
In one paragraph

Review in Biochemical Society transactions, 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

2 authors.

Elliott M BernardDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.
Ella HartenianDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.ORCID 0000-0001-9277-2152

Funding

Novartis AG | Novartis Consumer Health 24C168Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (SNF) PZ00-3_233297
6 · The paper itself

Abstract

Cell death pathways are ancient strategies that maintain homeostasis and protect organisms from infection and injury. Lytic cell death culminates in the rupture of the plasma membrane, which was recently revealed to be driven by Ninjurin-1 (NINJ1), a plasma membrane protein that oligomerizes during cell death. NINJ1 oligomerization creates lesions in the plasma membrane that facilitate the release of cytosolic contents. In the present review, we discuss what is currently known about NINJ1 biology, focusing on the most current research into potential mechanisms of activation. We then highlight how NINJ1 has been implicated in specific disease contexts and discuss potential ways NINJ1 may contribute to disease. We conclude with the remaining open questions relating to NINJ1 biology.

Indexed as

Cell Adhesion Molecules, NeuronalCell MembraneNerve Growth FactorsAnimalsCell DeathHumansCell Adhesion Molecules, NeuronalNerve Growth FactorsNINJ1 protein, humancell deathimmunologyinflammationNinj1

Identifiers

PMID42757451
PMCPMC13591262

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.