Evidence map›Paper›PMID 38842774›Full record

ArticleCurrent medical science2024

TL1A Promotes Fibrogenesis in Colonic Fibroblasts via the TGF-β1/Smad3 Signaling Pathway.

Jia Song, Dong-Lei Sun, Chen-Yang Li, Yu-Xin Luo, Qian Liu, Yue Yao, Hong Zhang, Ting-Ting Yang, Mei Song, Xin-Li Bai and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Tumor necrosis factor-like cytokine 1 A antagonists for inflammatory bowel disease: A systematic review and meta-analysis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. TL1A Inhibition in Inflammatory Bowel Disease: A Pipeline Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  11. Drug Development in Inflammatory Bowel Diseases: What Is Next?Pharmaceuticals (Basel, Switzerland) · 2025
    Review
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

11 authors.

Jia SongDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Dong-Lei SunDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Chen-Yang LiDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Yu-Xin LuoDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Qian LiuDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Yue YaoDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Hong ZhangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Ting-Ting YangDepartment of Pediatrics, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Mei SongDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China.
Xin-Li BaiDepartment of Pediatrics, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China. sindywhite@163.com.
Xiao-Lan ZhangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Institute of Gastroenterology, Hebei Clinical Research Center for Digestive Diseases, Shijiazhuang, 050000, China. xiaolanzh@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIntestinal fibrosis is a refractory complication of inflammatory bowel disease (IBD). Tumor necrosis factor ligand-related molecule-1A (TL1A) is important for IBD-related intestinal fibrosis in a dextran sodium sulfate (DSS)-induced experimental colitis model. This study aimed to explore the effects of TL1A on human colonic fibroblasts.

methodsA trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis model of LCK-CD2-TL1A-GFP transgenic (Tg) or wild-type (WT) mice was established to determine the effect and mechanism of TL1A on intestinal fibrosis. The human colonic fibroblast CCD-18Co cell line was treated concurrently with TL1A and human peripheral blood mononuclear cell (PBMC) supernatant. The proliferation and activation of CCD-18Co cells were detected by BrdU assays, flow cytometry, immunocytochemistry and Western blotting. Collagen metabolism was tested by Western blotting and real-time quantitative polymerase chain reaction (RT-qPCR).

resultsThe level of collagen metabolism in the TNBS+ethyl alcohol (EtOH)/Tg group was greater than that in the TNBS+EtOH/WT group. Transforming growth factor-β1 (TGF-β1) and p-Smad3 in the TNBS+EtOH/Tg group were upregulated as compared with those in the TNBS+EtOH/WT group. The proliferation of CCD-18Co cells was promoted by the addition of human PBMC supernatant supplemented with 20 ng/mL TL1A, and the addition of human PBMC supernatant and TL1A increased CCD-18Co proliferation by 24.4% at 24 h. TL1A promoted cell activation and increased the levels of COL1A2, COL3A1, and TIMP-1 in CCD-18Co cells. Treatment of CCD-18Co cells with TL1A increased the expression of TGF-β1 and p-Smad3.

conclusionTL1A promotes TGF-β1-mediated intestinal fibroblast activation, proliferation, and collagen deposition and is likely related to an increase in the TGF-β1/Smad3 signaling pathway.

Indexed as

Cell ProliferationFibroblastsFibrosisSignal TransductionSmad3 ProteinTransforming Growth Factor beta1Tumor Necrosis Factor Ligand Superfamily Member 15AnimalsCell LineColitisColonDisease Models, AnimalHumansLeukocytes, MononuclearMiceMice, TransgenicSmad3 ProteinSMAD3 protein, humanTGFB1 protein, humanTNFSF15 protein, humanTnfsf15 protein, mouseTransforming Growth Factor beta1Trinitrobenzenesulfonic AcidTumor Necrosis Factor Ligand Superfamily Member 15fibrosisinflammatory bowel diseasemyofibroblaststransforming growth factor-β1tumor necrosis factor ligand-related molecule-1A

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Registered trials

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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.