Evidence map›Paper›PMID 24850427›Full record

Trial reportMucosal immunology2014

Defective expression of SIRT1 contributes to sustain inflammatory pathways in the gut.

R Caruso, I Marafini, E Franzè, C Stolfi, F Zorzi, I Monteleone, F Caprioli, A Colantoni, M Sarra, S Sedda and 6 more

Open access · bronzeAbstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

64 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. The multifaceted role of sirtuins in inflammatory bowel diseases.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

4 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

16 authors at 2 institutions in 2 countries.

R CarusoDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
I MarafiniDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
E FranzèDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
C StolfiDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
F ZorziDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
I MonteleoneDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
F CaprioliUnit of Gastroenterology, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy.
A ColantoniDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
M SarraDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
S SeddaDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
L BianconeDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
P SileriDepartment of Surgery, University of Rome "Tor Vergata", Rome, Italy;
G S SicaDepartment of Surgery, University of Rome "Tor Vergata", Rome, Italy;
T T MacDonaldBarts and the London School of Medicine and Dentistry, London, UK.
F PalloneDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
G MonteleoneDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
University of Rome Tor Vergata · ITQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In inflammatory bowel disease (IBD), tissue damage is driven by an excessive immune response, poorly controlled by counter-regulatory mechanisms. SIRT1, a class III NAD+-dependent deacetylase, regulates negatively the expression of various proteins involved in the control of immune-inflammatory pathways, such as Stat3, Smad7, and NF-κB. Here we examined the expression, regulation, and function of SIRT1 in IBD. SIRT1 RNA and protein expression was less pronounced in whole biopsies and lamina propria mononuclear cells (LPMCs) of IBD patients in comparison with normal controls. SIRT1 expression was downregulated in control LPMC by tumor necrosis factor (TNF)-α and interleukin (IL)-21, and upregulated in IBD LPMC by neutralizing TNF-α and IL-21antibodies. Consistently, SIRT1 expression was increased in mucosal samples taken from IBD patients successfully treated with Infliximab. Treatment of IBD LPMC with Cay10591, a specific SIRT1 activator, reduced NF-κB activation and inhibited inflammatory cytokine synthesis, whereas Ex527, an inhibitor of SIRT1, increased interferon (IFN)-γ in control LPMC. SIRT1 was also reduced in mice with colitis induced by 2,4,6-trinitrobenzenesulphonic acid or oxazolone. Cay10591 prevented and cured experimental colitis whereas Ex527 exacerbated disease by modulating T cell-derived cytokine response. Data indicate that SIRT1 is downregulated in IBD patients and colitic mice and suggest that SIRT1 activation can help attenuate inflammatory signals in the gut.

Indexed as

Adjuvants, ImmunologicAdultAgedAged, 80 and overAnimalsAntibodies, MonoclonalAnti-Inflammatory Agents, Non-SteroidalFemaleGene Expression Regulation, EnzymologicHumansInflammatory Bowel DiseasesInfliximabInterferon-gammaInterleukin-21InterleukinsIntestinesAdjuvants, ImmunologicAntibodies, MonoclonalAnti-Inflammatory Agents, Non-SteroidalIFNG protein, humanInfliximabInterferon-gammaInterleukin-21InterleukinsOxazoloneSIRT1 protein, humanSirt1 protein, mouseSirtuin 1Trinitrobenzenesulfonic AcidTumor Necrosis Factor-alpha

Identifiers

PMID24850427
OpenAlexW2018707752

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.