Evidence map›Paper›PMID 37465675›Full record

ReviewFrontiers in immunology2023

TNF superfamily control of tissue remodeling and fibrosis.

Hope Steele, Jason Cheng, Ashley Willicut, Garrison Dell, Joey Breckenridge, Erica Culberson, Andrew Ghastine, Virginie Tardif, Rana Herro

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
17.1field-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

42 citing papers in PubMed, 66 citations in OpenAlex.

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  12. Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026
    Review
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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

9 authors at 4 institutions in 2 countries.

Hope SteeleDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Jason ChengDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Ashley WillicutUniversity of Cincinnati College of Medicine, Cincinnati, OH, United States.
Garrison DellDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Joey BreckenridgeDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Erica CulbersonUniversity of Cincinnati College of Medicine, Cincinnati, OH, United States.
Andrew GhastineDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Virginie TardifNormandy University, UniRouen, Institut National de la Santé et de la Recherche Médicale (INSERM), UMR1096 (EnVI Laboratory), Rouen, France.
Rana HerroDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · USUniversity of Cincinnati Medical Center · USInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is the result of extracellular matrix protein deposition and remains a leading cause of death in USA. Despite major advances in recent years, there remains an unmet need to develop therapeutic options that can effectively degrade or reverse fibrosis. The tumor necrosis super family (TNFSF) members, previously studied for their roles in inflammation and cell death, now represent attractive therapeutic targets for fibrotic diseases. In this review, we will summarize select TNFSF and their involvement in fibrosis of the lungs, the heart, the skin, the gastrointestinal tract, the kidney, and the liver. We will emphasize their direct activity on epithelial cells, fibroblasts, and smooth muscle cells. We will further report on major clinical trials targeting these ligands. Whether in isolation or in combination with other anti-TNFSF member or treatment, targeting this superfamily remains key to improve efficacy and selectivity of currently available therapies for fibrosis.

Indexed as

Epithelial CellsKidneyFibrosisHumansInflammationLungfibrosismucosaremodelingTNFSFTNF superfamily

Identifiers

PMID37465675
PMCPMC10351606
OpenAlexW4382984572

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.