Evidence map›Paper›PMID 41672970›Full record

ArticleCell death & disease2026

Loss of MLKL impairs abdominal aortic aneurysm development by attenuating smooth muscle cell necroptosis.

Harshal Nemade, Dennis Mehrkens, Hannah Sophia Lottermoser, Zeynep Ece Yilmaz, Julian Mader, Patrik Schelemei, Felix Ruben Picard, Simon Geißen, Gülsah Fülgen Schwab, Friedrich Felix Hoyer and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 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. Article
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

21 authors.

Harshal Nemade *Department for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany. hnemade@uni-koeln.de.ORCID http://orcid.org/0000-0002-2704-181X
Dennis Mehrkens *Department for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Hannah Sophia LottermoserDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Zeynep Ece YilmazDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Julian MaderDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0005-8892-1991
Patrik SchelemeiDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Felix Ruben PicardDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Simon GeißenDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Gülsah Fülgen SchwabDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Friedrich Felix HoyerDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Henning GuthoffDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Alexander HofDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Felix Sebastian NettersheimDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Agapios SachinidisCenter for Molecular Medicine Cologne (CMMC), Faculty of Medicine and Faculty of Mathematics and Natural Sciences, University of Cologne, Cologne, Germany.
Norbert GerdesDivision of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty and University Hospital, Heinrich-Heine University, Düsseldorf, Germany.
Gerhard SengleCenter for Molecular Medicine Cologne (CMMC), Faculty of Medicine and Faculty of Mathematics and Natural Sciences, University of Cologne, Cologne, Germany.
Holger WinkelsDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Stefan BaldusDepartment for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Manolis PasparakisCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Martin Mollenhauer *Department for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.
Matti Adam *Department for Experimental Cardiology, Faculty of Medicine, University of Cologne, and Clinic III for Internal Medicine, University Hospital Cologne, Cologne, Germany.

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 360043781Deutsche Forschungsgemeinschaft (German Research Foundation) 397484323Deutsche Forschungsgemeinschaft (German Research Foundation) 427806116Deutsche Forschungsgemeinschaft (German Research Foundation) HO 5279/2-1Else Kröner-Fresenius-Stiftung (Else Kroner-Fresenius Foundation) 2021_EKEA.83
6 · The paper itself

Abstract

Abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by chronic vascular inflammation and progressive aortic wall deterioration. MLKL-driven necroptosis, a highly inflammatory form of cell death, has been implicated in several cardiovascular pathologies; however, its role in AAA remains incompletely understood. Using the aortic elastase-perfusion model, we investigated the impact of necroptosis deficiency on AAA progression in necroptosis-deficient transgenic mice, including RIPK1 kinase-inactive (Ripk1

Indexed as

Aortic Aneurysm, AbdominalMyocytes, Smooth MuscleNecroptosisProtein KinasesAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutReceptor-Interacting Protein Serine-Threonine KinasesMLKL protein, mouseProtein KinasesReceptor-Interacting Protein Serine-Threonine Kinases

Identifiers

PMID41672970
PMCPMC12920694

What OpenQuestion holds

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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.