Evidence map›Paper›PMID 41353199›Full record

ArticleNature communications2025

A JAK/STAT-Pdk1-S6K axis bypasses systemic growth restrictions to promote regeneration.

Ananthakrishnan Vijayakumar Maya, Lena Neuhaus, Liyne Nogay, Aakriti Singh, Lara Heckmann, Isabelle Grass, Jörg Büscher, Katrin Kierdorf, Anne-Kathrin Classen

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

9 authors.

Ananthakrishnan Vijayakumar MayaHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0001-9698-0602
Lena NeuhausSpemann Graduate School of Biology and Medicine (SGBM), University of Freiburg, Freiburg, Germany.
Liyne NogayHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany.
Aakriti SinghHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0009-0006-7130-5022
Lara HeckmannHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0003-1264-9715
Isabelle GrassHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany.
Jörg BüscherMax Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.ORCID http://orcid.org/0000-0002-6547-0076
Katrin KierdorfInstitute of Neuropathology, Faculty of Medicine, Medical Center, University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0002-9272-4780
Anne-Kathrin ClassenHilde-Mangold-Haus, University of Freiburg, Freiburg, Germany. anne.classen@biologie.uni-freiburg.de.ORCID http://orcid.org/0000-0001-5157-0749

Funding

Boehringer Ingelheim Stiftung (Boehringer Ingelheim Foundation) Plus3Boehringer Ingelheim Stiftung (Boehringer Ingelheim Foundation) RiseUp!Deutsche Forschungsgemeinschaft (German Research Foundation) 529943809Deutsche Forschungsgemeinschaft (German Research Foundation) 544402801Deutsche Forschungsgemeinschaft (German Research Foundation) 667603Deutsche Forschungsgemeinschaft (German Research Foundation) 668189Deutsche Forschungsgemeinschaft (German Research Foundation) CIBSS - EXC-2189
6 · The paper itself

Abstract

Inflammation triggers systemic growth restrictions, a process well characterised in tumour cachexia. Whether inflammatory tissue damage also induces growth restrictions, and how regenerating tissue overcome them, is less explored. Using a tissue damage model in Drosophila, we identify metabolic and signaling adaptations that both induce and bypass systemic growth restrictions. Expression of eiger, the Drosophila TNF-α homolog, in imaginal discs causes systemic insulin restriction and insulin resistance, reducing protein translation and proliferation in peripheral tissues. Regenerating cells overcome this by upregulating Pdk1, which is necessary and sufficient to promote protein translation via an Insulin/Akt-independent mechanism. JAK/STAT acts upstream to elevate Pdk1, defining a JAK/STAT-Pdk1-S6K axis essential for regenerative proliferation. Regenerating cells also upregulate amino acid transporters and rely on mTORC1. Similar signatures in Ras

Indexed as

Drosophila ProteinsJanus KinasesProtein Serine-Threonine KinasesRegenerationSTAT Transcription FactorsAnimalsCell ProliferationDrosophila melanogasterImaginal DiscsInsulinInsulin ResistanceMechanistic Target of Rapamycin Complex 1Signal TransductionTranscription FactorsTumor Suppressor ProteinsDrosophila Proteinshop protein, DrosophilaInsulinJanus KinasesMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine KinasesSTAT Transcription FactorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID41353199
PMCPMC12686489

What Socratic 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 Socratic graph.