Evidence map›Paper›PMID 38052799›Full record

ArticleNature communications2023

The AMPK-Sirtuin 1-YAP axis is regulated by fluid flow intensity and controls autophagy flux in kidney epithelial cells.

Aurore Claude-Taupin, Pierre Isnard, Alessia Bagattin, Nicolas Kuperwasser, Federica Roccio, Biagina Ruscica, Nicolas Goudin, Meriem Garfa-Traoré, Alice Regnier, Lisa Turinsky and 8 more

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  4. Article
  5. Article
  6. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  7. Review
  8. Review
  9. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
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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

18 authors at 4 institutions in 1 country.

Aurore Claude-TaupinUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France. aurore.claude-taupin@inserm.fr.ORCID 0000-0002-0792-4295
Pierre IsnardUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Alessia BagattinUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Nicolas KuperwasserStructure Fédérative de Recherche Necker, US24-UMS3633, Paris, France.
Federica RoccioUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Biagina RuscicaUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Nicolas GoudinStructure Fédérative de Recherche Necker, US24-UMS3633, Paris, France.ORCID 0000-0002-3967-4016
Meriem Garfa-TraoréStructure Fédérative de Recherche Necker, US24-UMS3633, Paris, France.
Alice RegnierUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Lisa TurinskyUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.ORCID 0000-0002-2111-8521
Martine BurtinUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Marc ForetzInstitut Cochin, Inserm U1016 - CNRS UMR8104 - Université Paris Cité, 75014, Paris, France.ORCID 0000-0001-7017-9032
Marco PontoglioUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.ORCID 0000-0002-0617-7275
Etienne MorelUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.ORCID 0000-0002-4763-4954
Benoit ViolletInstitut Cochin, Inserm U1016 - CNRS UMR8104 - Université Paris Cité, 75014, Paris, France.ORCID 0000-0002-0121-0224
Fabiola TerziUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.
Patrice CodognoUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France.ORCID 0000-0002-5492-3180
Nicolas DupontUniversité Paris Cité, INSERM UMR-S1151, CNRS UMR-S8253, Institut Necker Enfants Malades, F-75015, Paris, France. nicolas.dupont@inserm.fr.ORCID 0000-0002-3056-9906
Centre National de la Recherche Scientifique · FRHôpital Necker-Enfants Malades · FRStructure fédérative de recherche Necker · FRInstitut Necker Enfants Malades · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shear stress generated by urinary fluid flow is an important regulator of renal function. Its dysregulation is observed in various chronic and acute kidney diseases. Previously, we demonstrated that primary cilium-dependent autophagy allows kidney epithelial cells to adapt their metabolism in response to fluid flow. Here, we show that nuclear YAP/TAZ negatively regulates autophagy flux in kidney epithelial cells subjected to fluid flow. This crosstalk is supported by a primary cilium-dependent activation of AMPK and SIRT1, independently of the Hippo pathway. We confirm the relevance of the YAP/TAZ-autophagy molecular dialog in vivo using a zebrafish model of kidney development and a unilateral ureteral obstruction mouse model. In addition, an in vitro assay simulating pathological accelerated flow observed at early stages of chronic kidney disease (CKD) activates YAP, leading to a primary cilium-dependent inhibition of autophagic flux. We confirm this YAP/autophagy relationship in renal biopsies from patients suffering from diabetic kidney disease (DKD), the leading cause of CKD. Our findings demonstrate the importance of YAP/TAZ and autophagy in the translation of fluid flow into cellular and physiological responses. Dysregulation of this pathway is associated with the early onset of CKD.

Indexed as

Renal Insufficiency, ChronicSirtuin 1AMP-Activated Protein KinasesAnimalsAutophagyEpithelial CellsHumansKidneyMiceZebrafishAMP-Activated Protein KinasesSirtuin 1

Identifiers

PMID38052799
PMCPMC10698145
OpenAlexW4389333357

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.