Evidence map›Paper›PMID 27250564›Full record

ReviewThe FEBS journal2016

Death in the intestinal epithelium-basic biology and implications for inflammatory bowel disease.

J Magarian Blander

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
16.2field-weighted citation impact, top 1% of its field
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

115 citing papers in PubMed, 191 citations in OpenAlex.

  1. Article
  2. iScience · 2026
    Article
  3. Article
  4. Review
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  16. Review
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  20. Article

55 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

J Magarian BlanderImmunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

THE ROLE OF ICSBP IN MUCOSAL IMMUNE RESPONSEP01DK072201 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HARPAZ, NOAM · 2006 to 2015
$14.6M
The Regulatory Control Mechanisms of Cross-presentation by Toll-like ReceptorsR01AI073899 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLANDER, JULIE MAGARIAN · 2008 to 2012
$2.1M
Non-Canonical Cross-presentation in Dendritic Cells Upon TAP BlockadeR01AI123284 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLANDER, JULIE MAGARIAN · 2016 to 2020
$2.1M
Control of protective immunity by innate pathways sensing bacterial viabilityR01AI095245 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLANDER, JULIE MAGARIAN · 2012 to 2015
$1.7M
Role of apoptosis in the intestinal epithelium during homeostasis and diseaseR01DK111862 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLANDER, JULIE MAGARIAN · 2017 to 2020
$1.5M
NIAID NIH HHS R01 AI073899NIAID NIH HHS R01 AI095245NIAID NIH HHS R01 AI123284NIDDK NIH HHS P01 DK072201NIDDK NIH HHS R01 DK111862
6 · The paper itself

Abstract

Every 4-5 days, intestinal epithelial cells (IEC) are terminated as they reach the end of their life. This process ensures that the epithelium is comprised of the fittest cells that maintain an impermeable barrier to luminal contents and the gut microbiota, as well as the most metabolically able cells that conduct functions in nutrient absorption, digestion, and secretion of antimicrobial peptides. IEC are terminated by apical extrusion-or shedding-from the intestinal epithelial monolayer into the gut lumen. Whether death by apoptosis signals extrusion or death follows expulsion by younger IEC has been a matter of debate. Seemingly a minor detail, IEC death before or after apical extrusion bears weight on the potential contribution of apoptotic IEC to intestinal homeostasis as a consequence of their recognition by intestinal lamina propria phagocytes. In inflammatory bowel disease (IBD), excessive death is observed in the ileal and colonic epithelium. The precise mode of IEC death in IBD is not defined. A highly inflammatory milieu within the intestinal lamina propria, rich in the proinflammatory cytokine, TNF-α, increases IEC shedding and compromises barrier integrity fueling more inflammation. A milestone in the treatment of IBD, anti-TNF-α therapy, may promote mucosal healing by reversing increased and inflammation-associated IEC death. Understanding the biology and consequences of cell death in the intestinal epithelium is critical to the design of new avenues for IBD therapy.

Indexed as

AnimalsCell CycleCell DeathHomeostasisHumansInflammatory Bowel DiseasesIntestinal MucosaModels, BiologicalTumor Necrosis Factor-alphaTumor Necrosis Factor-alphaapoptosisinflammatory bowel diseaseintestinal epithelial cellintestinal tolerancetumor necrosis factor

Identifiers

PMID27250564
PMCPMC4956528
OpenAlexW2411014978

What OpenQuestion holds

Textmetadata
LicenceTDM
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.