Evidence map›Paper›PMID 39489847›Full record

ArticlePediatric surgery international2024

Dissecting the dynamics of cell death pathways in Hirschsprung's disease: a comparative analysis of viable and non-viable cells under proinflammatory conditions.

Zhongwen Li, Johanna Hagens, Clara Philippi, Hans Christian Schmidt, Lucie Rohwäder, Pauline Schuppert, Laia Pagerols Raluy, Magdalena Trochimiuk, Konrad Reinshagen, Christian Tomuschat

Abstract readComparative Study
In one paragraph

Article in Pediatric surgery international, 2024. 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

10 authors.

Zhongwen Li *Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Johanna Hagens *Department of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Clara PhilippiDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hans Christian SchmidtDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Lucie RohwäderDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Pauline SchuppertDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Laia Pagerols RaluyDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Magdalena TrochimiukDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Konrad ReinshagenDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Christian TomuschatDepartment of Pediatric Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. c.tomuschat@uke.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe present study explores the dynamics of cell death in Hirschsprung's disease (HSCR) and control (CO) groups under inflammatory stress conditions.

methodsUsing flow cytometry, we analyzed intestinal colonic organoid cultures derived from the ganglionic segment of the HSCR and CO groups. Our analysis focused on the quantification of RIPK1-independent and RIPK1-dependent apoptosis, as well as necroptosis in both viable and non-viable cells under acute and chronic inflammatory stress.

resultsOur findings indicate that HSCR cells are particularly vulnerable to inflammation during acute proinflammatory stress, as evidenced by an increase in dead cells (Zombie +). Under chronic conditions, adaptive changes are observed in both HSCR and CO groups, indicating survival mechanisms. These adaptations are uniquely altered in HSCR, suggesting an impaired response to chronic inflammation. HSCR cells show significantly decreased RIPK1-dependent apoptosis in acute scenarios compared to chronic ones, unlike the CO group, implying varied responses to different inflammatory stresses. In non-viable cells, considerable changes in RIPK1-dependent apoptosis under chronic conditions in HSCR indicate a heightened inflammatory response compared to CO.

conclusionThis research provides insights into cell death regulation in HSCR under inflammatory stress by using patient-derived organoids, underscoring the complexity of its inflammatory response.

Indexed as

ApoptosisHirschsprung DiseaseInflammationCell DeathColonFemaleFlow CytometryHumansInfantMaleNecroptosisOrganoidsReceptor-Interacting Protein Serine-Threonine KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanApoptosisHirschsprung’s diseaseNecroptosisOrganoidsRIK1RIP3–caspase-3 assay

Identifiers

PMID39489847
PMCPMC11532316

What OpenQuestion holds

Textmetadata
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.