ArticleMucosal immunology2014
Targeting sirtuin-1 alleviates experimental autoimmune colitis by induction of Foxp3+ T-regulatory cells.
Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Survival and Clinicopathological Significance of SIRT1 Expression in Cancers: A Meta-Analysis.Frontiers in endocrinology · 2019Pooled it
- Defective expression of SIRT1 contributes to sustain inflammatory pathways in the gut.Mucosal immunology · 2014Trial
- Human umbilical cord mesenchymal stem cell-derived exosomes repair IBD by activating the SIRT1-FXR pathway in macrophages.Stem cell research & therapy · 2025Article
- Inhibition SIRT1 to regulate FOXP3 or RORγt can restore the balance of Treg/Th17 axis in ulcerative colitis and enhance the anti-inflammatory effect of moxibustion.Frontiers in immunology · 2024Article
- Reproductive Immunology and Pregnancy 3.0.International journal of molecular sciences · 2023Article
- NADAntioxidants (Basel, Switzerland) · 2023Review
- The poly(C)-binding protein Pcbp2 is essential for CD4iScience · 2023Article
- PRMT5 regulates epigenetic changes in suppressive Th1-like iTregs in response to IL-12 treatment.Frontiers in immunology · 2023Article
- T cells in abdominal aortic aneurysm: immunomodulation and clinical application.Frontiers in immunology · 2023Review
- Columbianadin attenuates doxorubicin-induced cardiac injury, oxidative stress, and apoptosis via Sirt1/FOXO1 signaling pathway.Acta cirurgica brasileira · 2023Article
- Sirtuin family in autoimmune diseases.Frontiers in immunology · 2023Review
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- Article
- SIRT1: A Potential Therapeutic Target in Autoimmune Diseases.Frontiers in immunology · 2021Review
- Protection against Doxorubicin-Related Cardiotoxicity by Jaceosidin Involves the Sirt1 Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Immune and microRNA responses toWorld journal of gastroenterology · 2020Article
- Histone Deacetylation Inhibitors as Modulators of Regulatory T Cells.International journal of molecular sciences · 2020Review
- The stress polarity signaling (SPS) pathway serves as a marker and a target in the leaky gut barrier: implications in aging and cancer.Life science alliance · 2020Article
- The Fate of Th17 Cells is Shaped by Epigenetic Modifications and Remodeled by the Tumor Microenvironment.International journal of molecular sciences · 2020Review
- HDAC10 deletion promotes Foxp3Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Induced Forkhead box P3-positive (Foxp3(+)) T-regulatory cells (iTregs) are essential to gastrointestinal immune homeostasis, and loss of the ability to develop iTregs may lead to autoimmune colitis. We previously showed a role for sirtuin-1 (Sirt1) in control of Treg function and hypothesized that targeting of Sirt1 might enhance iTreg development and thereby represent a potential therapy for inflammatory bowel disease (IBD). We adoptively transferred CD4(+)CD25(-)Foxp3(-) T effector (TE) cells from wild-type (WT) (C57BL/6) or fl-Sirt1/CD4cre mice into B6/Rag1(-/-) mice and monitored the mice until they lost 10-15% of their weight. Adoptive transfer of TE cells lacking Sirt1 to B6/Rag1(-/-) mice resulted in a 2.8-fold increase in iTreg formation compared with mice receiving WT TE cells and correlated with attenuated colitis and reduced weight loss (1.04±1.4% vs. 13.97±2.2%, respectively, P<0.001). In a second model of IBD, we used pharmacologic Sirt1 targeting of mice receiving multiple cycles of dextran sodium sulfate (DSS) in their drinking water, alternated with fresh water. Likewise, WT mice receiving cyclic DSS and a Sirt1 inhibitor, EX-527, had reduced weight loss (5.8±5.9% vs. 13.2±6.9%, respectively, P=0.03) and increased iTreg formation compared with controls. Sirt1 appears a promising target for pharmacologic therapy of IBD as a result of promoting iTreg development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.