Evidence map›Paper›PMID 26823555›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

A Novel Extrinsic Pathway for the Unfolded Protein Response in the Kidney.

Iadh Mami, Quentin Tavernier, Nicolas Bouvier, Rim Aboukamis, Geoffroy Desbuissons, Marion Rabant, Virginie Poindessous, Pierre Laurent-Puig, Philippe Beaune, Pierre-Louis Tharaux and 4 more

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Linking cellular stress responses to systemic homeostasis.Nature reviews. Molecular cell biology · 2018
    Review
  19. Article
  20. 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

14 authors at 7 institutions in 2 countries.

Iadh MamiInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France;
Quentin TavernierInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France;
Nicolas BouvierService de Néphrologie, Centre Hospitalier Unversitaire de Caen, Caen, France;
Rim AboukamisInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France;
Geoffroy DesbuissonsUniversité Paris Descartes, Paris, France; Service de Néphrologie, INSERM U1151, Institut Necker Enfants Malades, Paris, France;
Marion RabantUniversité Paris Descartes, Paris, France; Service d'Anatomopathologie, Hôpital Necker, Paris, France;
Virginie PoindessousInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France;
Pierre Laurent-PuigInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France; Service de Biochimie, Service de Néphrologie, Hôpital Européen Georges Pompidou, Paris, France;
Philippe BeauneInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France; Service de Biochimie, Service de Néphrologie, Hôpital Européen Georges Pompidou, Paris, France;
Pierre-Louis TharauxParis Cardiovascular Research Center, INSERM, Paris, France; and.
Eric ThervetUniversité Paris Descartes, Paris, France; Service de Néphrologie, Centre Hospitalier Unversitaire de Caen, Caen, France; Service de Néphrologie, Centre Hospitalier Unversitaire de Caen, Caen, France;
Eric ChevetOncogenesis Stress Signaling Laboratory, ER440 INSERM, Université de Rennes 1, Centre de Lutte Contre le Cancer Eugène Marquis, Rennes, France.
Dany AnglicheauUniversité Paris Descartes, Paris, France; Service de Néphrologie, INSERM U1151, Institut Necker Enfants Malades, Paris, France;
Nicolas PalletInstitut National de la Santé et de le Recherche Médicale (INSERM) U1147, Centre Universitaire des Saints Pères, Paris, France; Université Paris Descartes, Paris, France; Service de Biochimie, Service de Néphrologie, Hôpital Européen Georges Pompidou, Paris, France; npallet@yahoo.fr.
Délégation Paris 5 · FRInserm · FRUniversité Paris Cité · FRCentre Hospitalier Universitaire de Caen · FRHôpital Européen · FRHôpital Necker-Enfants Malades · FRParis Cardiovascular Research Center · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ribonuclease angiogenin is a component of the mammalian stress response, and functions in both cell-autonomous and non-cell-autonomous ways to promote tissue adaptation to injury. We recently showed that angiogenin regulates tissue homeostasis during AKI associated with endoplasmic reticulum (ER) stress through the production of transfer RNA fragments that interfere with translation initiation and thereby alleviate ER stress. However, whether the paracrine signaling mediated by angiogenin secretion is a genuine component of the ER stress response to kidney injury is unknown. Here, we explored the molecular mechanisms by which angiogenin is secreted upon ER stress, and determined how it modulates the inflammatory microenvironment. In cultured renal epithelial cells, ER stress specifically induced angiogenin secretion under the selective control of inositol-requiring enzyme 1α, a key activator of the unfolded protein response. The transcription factors spliced X-box-binding protein 1 and p65, which are activated by inositol-requiring enzyme 1α upon ER stress, each bound the angiogenin promoter and controlled the amount of angiogenin secreted. Furthermore, p65 promoted angiogenin transcription in an ER stress-dependent manner. Similar to secretion of the ER stress-induced proinflammatory cytokine IL-6, secretion of angiogenin required the ER-Golgi pathway. Notably, incubation of human macrophages with angiogenin promoted macrophage reprogramming toward an activated and proinflammatory phenotype. In patients, angiogenin expression increased upon renal inflammation, and the urinary concentration of angiogenin correlated with the extent of immune-mediated kidney injury. Collectively, our data identify angiogenin as a mediator of the ER stress-dependent inflammatory response and as a potential noninvasive biomarker of AKI.

Indexed as

Signal TransductionAnimalsCells, CulturedEndoplasmic Reticulum StressKidneyMacrophagesMiceMice, Inbred C57BLRibonuclease, PancreaticUnfolded Protein ResponseangiogeninRibonuclease, Pancreaticacute rejectioncell activationcytokinesmacrophagesrenal tubular epithelial cells

Identifiers

PMID26823555
PMCPMC5004651
OpenAlexW2258244770

What OpenQuestion holds

Textmetadata
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.