Evidence map›Paper›PMID 38559587›Full record

ArticleJournal of oral biology and craniofacial research

Cell type-specific transforming growth factor-β (TGF-β) signaling in the regulation of salivary gland fibrosis and regeneration.

Kevin Muñoz Forti, Gary A Weisman, Kimberly J Jasmer

Open access · goldAbstract read
In one paragraph

Article in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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  6. 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

3 authors at 1 institution in 1 country.

Kevin Muñoz FortiChristopher S. Bond Life Sciences Center and Department of Biochemistry, University of Missouri, United States.
Gary A WeismanChristopher S. Bond Life Sciences Center and Department of Biochemistry, University of Missouri, United States.
Kimberly J JasmerChristopher S. Bond Life Sciences Center and Department of Biochemistry, University of Missouri, United States.
University of Missouri · US

Funding

Targeting P2 Receptors to Restore Salivary and Lacrimal Gland Function in Sjogren's SyndromeR01DE029833 · NIDCR · UNIVERSITY OF MISSOURI-COLUMBIA · PI WEISMAN, GARY ANDREW · 2021 to 2025
$3.2M
The P2X7 receptor for ATP as a therapeutic target in the prevention of radiation-induced salivary gland dysfunctionR01DE032032 · NIDCR · UNIVERSITY OF MISSOURI-COLUMBIA · PI GARY Andrew WEISMAN · 2023 to 2026
$2.1M
NIDCR NIH HHS R01 DE029833NIDCR NIH HHS R01 DE032032
6 · The paper itself

Abstract

Salivary gland damage and hypofunction result from various disorders, including autoimmune Sjögren's disease (SjD) and IgG4-related disease (IgG4-RD), as well as a side effect of radiotherapy for treating head and neck cancers. There are no therapeutic strategies to prevent the loss of salivary gland function in these disorders nor facilitate functional salivary gland regeneration. However, ongoing aquaporin-1 gene therapy trials to restore saliva flow show promise. To identify and develop novel therapeutic targets, we must better understand the cell-specific signaling processes involved in salivary gland regeneration. Transforming growth factor-β (TGF-β) signaling is essential to tissue fibrosis, a major endpoint in salivary gland degeneration, which develops in the salivary glands of patients with SjD, IgG4-RD, and radiation-induced damage. Though the deposition and remodeling of extracellular matrix proteins are essential to repair salivary gland damage, pathological fibrosis results in tissue hardening and chronic salivary gland dysfunction orchestrated by multiple cell types, including fibroblasts, myofibroblasts, endothelial cells, stromal cells, and lymphocytes, macrophages, and other immune cell populations. This review is focused on the role of TGF-β signaling in the development of salivary gland fibrosis and the potential for targeting TGF-β as a novel therapeutic approach to regenerate functional salivary glands. The studies presented highlight the divergent roles of TGF-β signaling in salivary gland development and dysfunction and illuminate specific cell populations in damaged or diseased salivary glands that mediate the effects of TGF-β. Overall, these studies strongly support the premise that blocking TGF-β signaling holds promise for the regeneration of functional salivary glands.

Indexed as

FibrosisHyposalivationRegenerationSalivary duct ligation modelSalivary glandsTGF-β signaling

Identifiers

PMID38559587
PMCPMC10979288
OpenAlexW4393032135

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.