Evidence map›Paper›PMID 35263141›Full record

ArticleScience advances2022

Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism.

Alexander S Häusl, Thomas Bajaj, Lea M Brix, Max L Pöhlmann, Kathrin Hafner, Meri De Angelis, Joachim Nagler, Frederik Dethloff, Georgia Balsevich, Karl-Werner Schramm and 4 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  6. Analgesia through FKBP51 inhibition at disease onset confers lasting relief from sensory and emotional chronic pain symptoms.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

14 authors at 4 institutions in 2 countries.

Alexander S HäuslResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany.ORCID 0000-0003-3305-5406
Thomas BajajNeurohomeostasis Research Group, Department of Psychiatry and Psychotherapy, Bonn Clinical Center, University of Bonn, 53127 Bonn, Germany.ORCID 0000-0001-6153-6608
Lea M BrixResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany.ORCID 0000-0002-3655-4385
Max L PöhlmannResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany.ORCID 0000-0003-2230-2846
Kathrin HafnerDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, 80804 Munich, Germany.
Meri De AngelisHelmholtz Center Munich Germany Research Center for Environmental Health, Molecular EXposomics, Neuherberg, Germany.
Joachim NaglerHelmholtz Center Munich Germany Research Center for Environmental Health, Molecular EXposomics, Neuherberg, Germany.
Frederik DethloffMax Planck Institute for Biology of Ageing, 50931 Cologne, Germany.
Georgia BalsevichResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany.
Karl-Werner SchrammHelmholtz Center Munich Germany Research Center for Environmental Health, Molecular EXposomics, Neuherberg, Germany.
Patrick GiavaliscoMax Planck Institute for Biology of Ageing, 50931 Cologne, Germany.ORCID 0000-0002-4636-1827
Alon ChenDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, 80804 Munich, Germany.ORCID 0000-0003-3625-8233
Mathias V SchmidtResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany.ORCID 0000-0002-3788-2268
Nils C GassenNeurohomeostasis Research Group, Department of Psychiatry and Psychotherapy, Bonn Clinical Center, University of Bonn, 53127 Bonn, Germany.ORCID 0000-0002-4265-3398
Max Planck Institute of Psychiatry · DEHelmholtz Zentrum München · DEMax Planck Institute for Biology of Ageing · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mediobasal hypothalamus (MBH) is the central region in the physiological response to metabolic stress. The FK506-binding protein 51 (FKBP51) is a major modulator of the stress response and has recently emerged as a scaffolder regulating metabolic and autophagy pathways. However, the detailed protein-protein interactions linking FKBP51 to autophagy upon metabolic challenges remain elusive. We performed mass spectrometry-based metabolomics of FKBP51 knockout (KO) cells revealing an increased amino acid and polyamine metabolism. We identified FKBP51 as a central nexus for the recruitment of the LKB1/AMPK complex to WIPI4 and TSC2 to WIPI3, thereby regulating the balance between autophagy and mTOR signaling in response to metabolic challenges. Furthermore, we demonstrated that MBH FKBP51 deletion strongly induces obesity, while its overexpression protects against high-fat diet (HFD)-induced obesity. Our study provides an important novel regulatory function of MBH FKBP51 within the stress-adapted autophagy response to metabolic challenges.

Indexed as

HypothalamusTacrolimus Binding ProteinsAutophagyDiet, High-FatHumansObesityTacrolimus Binding Proteins

Identifiers

PMID35263141
PMCPMC8906734
OpenAlexW4220927759

What OpenQuestion holds

Textmetadata
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.