Evidence map›Paper›PMID 34330919›Full record

ArticleNature communications2021

Stress-primed secretory autophagy promotes extracellular BDNF maturation by enhancing MMP9 secretion.

Silvia Martinelli, Elmira A Anderzhanova, Thomas Bajaj, Svenja Wiechmann, Frederik Dethloff, Katja Weckmann, Daniel E Heinz, Tim Ebert, Jakob Hartmann, Thomas M Geiger and 15 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
11.3field-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

73 citing papers in PubMed, 124 citations in OpenAlex.

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  19. The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025
    Review
  20. Well-being and biological cost of family members affected by substance use disorder of others.European archives of psychiatry and clinical neuroscience · 2025
    Article

13 more citing papers are in PubMed but not listed here.

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

25 authors at 5 institutions in 3 countries.

Silvia Martinelli *Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany. silviamartinelli@outlook.de.ORCID 0000-0002-8784-2213
Elmira A Anderzhanova *Research Group Neurohomeostasis, Department of Psychiatry and Psychotherapy, University of Bonn, Bonn, Germany.
Thomas BajajResearch Group Neurohomeostasis, Department of Psychiatry and Psychotherapy, University of Bonn, Bonn, Germany.
Svenja WiechmannChair of Proteomics and Bioanalytics, Technical University of Munich, Emil-Erlenmeyer-Forum 5, Freising, Germany.ORCID 0000-0003-1324-0743
Frederik DethloffDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Katja WeckmannDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Daniel E HeinzResearch Group Neurohomeostasis, Department of Psychiatry and Psychotherapy, University of Bonn, Bonn, Germany.ORCID 0000-0001-7103-9621
Tim EbertResearch Group Neurohomeostasis, Department of Psychiatry and Psychotherapy, University of Bonn, Bonn, Germany.
Jakob HartmannDepartment of Psychiatry, Harvard Medical School and McLean Hospital, Belmont, MA, USA.ORCID 0000-0002-1960-8177
Thomas M GeigerInstitute for Organic Chemistry and Biochemistry, Technische Universität Darmstadt, Darmstadt, Germany.
Michael DöngiInstitut für Physiologie II, University of Bonn, Bonn, Germany.
Kathrin HafnerDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Max L PöhlmannResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, Munich, Germany.
Lee JollansDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.ORCID 0000-0003-4254-5159
Alexandra PhilipsenDepartment of Psychiatry and Psychotherapy, University of Bonn, Bonn, Germany.
Susanne V SchmidtInstitute of Innate Immunity, University of Bonn, Bonn, Germany.
Ulrike SchmidtResearch Group Molecular and Clinical Psychotraumatology, Department of Psychiatry and Psychotherapy, Rheinische Friedrich-Wilhelms-Universität Bonn, Bonn, Germany.
Giuseppina MaccarroneDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Valentin SteinInstitut für Physiologie II, University of Bonn, Bonn, Germany.ORCID 0000-0003-1222-4928
Felix HauschInstitute for Organic Chemistry and Biochemistry, Technische Universität Darmstadt, Darmstadt, Germany.ORCID 0000-0002-3710-8838
Christoph W TurckDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Mathias V SchmidtResearch Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, Munich, Germany.ORCID 0000-0002-3788-2268
Anne-Kathrin GellnerInstitut für Physiologie II, University of Bonn, Bonn, Germany.
Bernhard KusterChair of Proteomics and Bioanalytics, Technical University of Munich, Emil-Erlenmeyer-Forum 5, Freising, Germany.ORCID 0000-0002-9094-1677
Nils C GassenDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany. nils.gassen@ukbonn.de.ORCID 0000-0002-4265-3398
University of Bonn · DEMax Planck Institute of Psychiatry · DEGerman Cancer Research Center · DETechnische Universität Darmstadt · DEHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The stress response is an essential mechanism for maintaining homeostasis, and its disruption is implicated in several psychiatric disorders. On the cellular level, stress activates, among other mechanisms, autophagy that regulates homeostasis through protein degradation and recycling. Secretory autophagy is a recently described pathway in which autophagosomes fuse with the plasma membrane rather than with lysosomes. Here, we demonstrate that glucocorticoid-mediated stress enhances secretory autophagy via the stress-responsive co-chaperone FK506-binding protein 51. We identify the matrix metalloproteinase 9 (MMP9) as one of the proteins secreted in response to stress. Using cellular assays and in vivo microdialysis, we further find that stress-enhanced MMP9 secretion increases the cleavage of pro-brain-derived neurotrophic factor (proBDNF) to its mature form (mBDNF). BDNF is essential for adult synaptic plasticity and its pathway is associated with major depression and posttraumatic stress disorder. These findings unravel a cellular stress adaptation mechanism that bears the potential of opening avenues for the understanding of the pathophysiology of stress-related disorders.

Indexed as

AnimalsAutophagosomesAutophagyBrain-Derived Neurotrophic FactorCell LineCell Line, TumorCell MembraneDexamethasoneGlucocorticoidsHEK293 CellsHumansMatrix Metalloproteinase 9MiceMice, KnockoutNeuronal PlasticitySignal TransductionBrain-Derived Neurotrophic FactorDexamethasoneGlucocorticoidsMatrix Metalloproteinase 9

Identifiers

PMID34330919
PMCPMC8324795
OpenAlexW3185482044

What OpenQuestion holds

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LicenceCC BY
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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.