Evidence map›Paper›PMID 31637864›Full record

ArticleAging cell2020

Systemic GDF11 stimulates the secretion of adiponectin and induces a calorie restriction-like phenotype in aged mice.

Lida Katsimpardi, Nicolas Kuperwasser, Claire Camus, Carine Moigneu, Aurélie Chiche, Virginie Tolle, Han Li, Erzsebet Kokovay, Pierre-Marie Lledo

Abstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Review
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  6. GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  7. Article
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  9. Review
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  11. Review
  12. GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  13. Article
  14. Article
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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

9 authors.

Lida KatsimpardiPerception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.ORCID 0000-0001-5688-7104
Nicolas KuperwasserDepartment of Cell Growth and Signaling, Institut National de la Santé et de la Recherche Médicale (INSERM) U1151, Institut Necker Enfants Malades (INEM), Université Paris Descartes, France.ORCID 0000-0002-7841-3214
Claire CamusPerception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.ORCID 0000-0003-0980-9917
Carine MoigneuPerception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.ORCID 0000-0002-4508-3108
Aurélie ChicheDepartment of Developmental & Stem Cell Biology, Cellular Plasticity & Disease Modelling, CNRS UMR 3738, Institut Pasteur, Paris, France.
Virginie TolleCentre de Psychiatrie et Neurosciences, UMR-S 894, INSERM, Université Paris Descartes Sorbonne Paris Cité, Paris, France.
Han LiDepartment of Developmental & Stem Cell Biology, Cellular Plasticity & Disease Modelling, CNRS UMR 3738, Institut Pasteur, Paris, France.
Erzsebet KokovayCell Systems and Anatomy, Brashop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Pierre-Marie LledoPerception and Memory Lab, Neuroscience Department, Institut Pasteur, Paris, France.ORCID 0000-0002-8156-7003

Funding

Agence Nationale de Recherche ANR-10-LABX-73Agence Nationale de Recherche ANR-11-IDEX-0004-02Agence Nationale de Recherche ANR-15-CE37-0004-01Barshop Institute Nathan Shock CenterMorrison Trust Foundation
6 · The paper itself

Abstract

Aging is a negative regulator of general homeostasis, tissue function, and regeneration. Changes in organismal energy levels and physiology, through systemic manipulations such as calorie restriction and young blood infusion, can regenerate tissue activity and increase lifespan in aged mice. However, whether these two systemic manipulations could be linked has never been investigated. Here, we report that systemic GDF11 triggers a calorie restriction-like phenotype without affecting appetite or GDF15 levels in the blood, restores the insulin/IGF-1 signaling pathway, and stimulates adiponectin secretion from white adipose tissue by direct action on adipocytes, while repairing neurogenesis in the aged brain. These findings suggest that GDF11 has a pleiotropic effect on an organismal level and that it could be a linking mechanism of rejuvenation between heterochronic parabiosis and calorie restriction. As such, GDF11 could be considered as an important therapeutic candidate for age-related neurodegenerative and metabolic disorders.

Indexed as

AdiponectinAgingAnimalsBone Morphogenetic ProteinsCaloric RestrictionGrowth Differentiation FactorsMicePhenotypeAdiponectinBone Morphogenetic ProteinsGdf11 protein, mouseGrowth Differentiation Factorsadiponectinagingcalorie restrictionGDF11heterochronic parabiosisrejuvenation

Identifiers

PMID31637864
PMCPMC6974718

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Registered trials

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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.