Evidence map›Paper›PMID 39803569›Full record

ArticlebioRxiv : the preprint server for biology2025

Rescue of non-healing, degenerative salivary glands by cholinergic-calcium signaling.

Jianlong Li, Bo Sun, Li Xuan Tan, Nathan Griffin, Seyyed Vahid Niknezhad, Chieh Yu, Lionel Berthoin, Noel Cruz-Pacheco, Seayar Mohabbat, Hanan Sinada and 7 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Jianlong LiDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA; School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao, China.
Bo SunDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Li Xuan TanDepartment of Ophthalmology, School of Medicine, University of California San Francisco, San Francisco, California, USA; School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao, China.
Nathan GriffinDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Seyyed Vahid NiknezhadDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Chieh YuDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Lionel BerthoinDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Noel Cruz-PachecoDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Seayar MohabbatDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Hanan SinadaDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Yael EfraimDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Feeling Yu Ting ChenDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Luye AnDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Eliza A GaylordDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.
Chelsey S BahneyUniversity of California, San Francisco. Orthopedic Trauma Institute, San Francisco, CA.ORCID 0000-0001-9808-8888
Isabelle M A LombaertBiointerfaces Institute, University of Michigan, Ann Arbor, Michigan, USA.ORCID 0000-0002-7547-6375
Sarah M KnoxDepartment of Cell and Tissue Biology, School of Dentistry, University of California San Francisco, San Francisco, California, USA.ORCID 0000-0002-7567-083X

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Center for Dental, Oral, and Craniofacial Tissue and Organ Regeneration (C-DOCTOR)U24DE026914 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAI, YANG, CHEN, YONG · 2017 to 2019
$12.0M
PREDOCTORAL TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007470 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Todd Nystul · 1994 to 2026
$7.7M
Defining mechanisms driving salivary gland regenerationR35DE028255 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KNOX, SARAH MONICA · 2018 to 2025
$7.7M
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
$573k
Cytek Aurora 5-Laser Spectral Flow CytometerS10OD026940 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SIMOES MARTINS BISPO, CLAUDIA · 2019 to 2019
$341k
NICHD NIH HHS T32 HD007470NIDCR NIH HHS R35 DE028255NIDCR NIH HHS U24 DE026914NIDDK NIH HHS P30 DK063720NIH HHS S10 OD021822NIH HHS S10 OD026940
6 · The paper itself

Abstract

Chronic degenerative wounds are often deemed irreparable, directing research efforts to focus predominantly on acute tissue injury regeneration while leaving endogenous repair mechanisms for chronically damaged tissues largely unexplored. In this study, we demonstrate that non-healing, severely degenerated salivary gland tissues can be fundamentally restored through first-line treatment with muscarinic agonists. This approach rescues tissue structure and function, returning it to a homeostatic-like state, and reactivates endogenous regeneration processes to drive new cell expansion that persists for months post-treatment. Furthermore, neuromimetic activation profoundly depletes radiation-induced DNA damage and re-establishes the nerve-acinar relationship, ultimately restoring the tissues physiological capacity to maintain homeostasis, even in the absence of treatment. We show that full recovery of organ function, comparable to uninjured controls, is primarily mediated by the re-differentiation of aberrantly de-differentiated epithelial acinar cells and the restoration of mitochondrial function via a muscarinic-calcium signaling pathway. These findings challenge the prevailing notion that chronic organ degeneration is irreversible and propose a readily testable therapeutic strategy for epithelial restoration with potential applications across a spectrum of chronic injuries.

Indexed as

calcium signalingcholinergicChronic degenerationepithelial wound healingmitochondrial metabolismorgan failureradiation therapysalivary glandtissue regeneration

Identifiers

PMID39803569
PMCPMC11722244

What OpenQuestion holds

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LicenceCC BY-NC
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.