Evidence map›Paper›PMID 37507441›Full record

ArticleNature communications2023

Modulating p38 MAPK signaling by proteostasis mechanisms supports tissue integrity during growth and aging.

Wang Yuan, Yi M Weaver, Svetlana Earnest, Clinton A Taylor, Melanie H Cobb, Benjamin P Weaver

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.4field-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

27 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. AScience signaling · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. International journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Gut commensalMicrobiology spectrum · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

6 authors at 1 institution in 1 country.

Wang YuanDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0003-1575-4596
Yi M WeaverDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA.
Svetlana EarnestDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA.
Clinton A TaylorDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA.
Melanie H CobbDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0003-0833-5473
Benjamin P WeaverDepartment of Pharmacology, UT Southwestern Medical Center, Dallas, TX, USA. Benjamin.Weaver@UTSouthwestern.edu.ORCID 0000-0002-0830-213X
Southwestern Medical Center · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeffrey M Zigman · 2022 to 2026
$7.4M
Proteolytic Mechanisms Mediating Diverse Non-Apoptotic Caspase FunctionsR35GM133755 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Benjamin P. Weaver · 2019 to 2026
$3.7M
NIDDK NIH HHS P30 DK127984NIGMS NIH HHS R35 GM133755NIGMS NIH HHS R35GM133755NIH HHS P40 OD010440
6 · The paper itself

Abstract

The conserved p38 MAPK family is activated by phosphorylation during stress responses and inactivated by phosphatases. C. elegans PMK-1 p38 MAPK initiates innate immune responses and blocks development when hyperactivated. Here we show that PMK-1 signaling is enhanced during early aging by modulating the stoichiometry of non-phospho-PMK-1 to promote tissue integrity and longevity. Loss of pmk-1 function accelerates progressive declines in neuronal integrity and lysosome function compromising longevity which has both cell autonomous and cell non-autonomous contributions. CED-3 caspase cleavage limits phosphorylated PMK-1. Enhancing p38 signaling with caspase cleavage-resistant PMK-1 protects lysosomal and neuronal integrity extending a youthful phase. PMK-1 works through a complex transcriptional program to regulate lysosome formation. During early aging, the absolute phospho-p38 amount is maintained but the reservoir of non-phospho-p38 diminishes to enhance signaling without hyperactivation. Our findings show that modulating the stoichiometry of non-phospho-p38 dynamically supports tissue-homeostasis during aging without hyper-activation of stress response.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsAgingAnimalsCaspasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProteostasisCaenorhabditis elegans ProteinsCaspasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinases

Identifiers

PMID37507441
PMCPMC10382525
OpenAlexW4385347917

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.