Evidence map›Paper›PMID 37667516›Full record

ArticleAging cell2023

Loss of Pla2r1 decreases cellular senescence and age-related alterations caused by aging and Western diets.

Amélie Massemin, Delphine Goehrig, Jean-Michel Flaman, Sara Jaber, Audrey Griveau, Sophia Djebali, Elisabeth Marcos, Léa Payen, Jacqueline Marvel, Romain Parent and 6 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

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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

16 authors at 3 institutions in 1 country.

Amélie MasseminCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Delphine GoehrigCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Jean-Michel FlamanCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Sara JaberCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Audrey GriveauCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Sophia DjebaliCentre International de Recherche en Infectiologie, Inserm U1111, CNRS UMR5308, École Normale Supérieure de Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.ORCID 0000-0002-0567-5387
Elisabeth MarcosINSERM U955, Département de Physiologie - Explorations fonctionnelles, Hôpital Henri Mondor, AP-HP, FHU SENEC, Créteil, France.
Léa PayenLaboratoire de Biochimie et Biologie Moléculaire, Centre Hospitalier Lyon Sud, Hospices Civils de Lyon, Pierre Bénite, France.
Jacqueline MarvelCentre International de Recherche en Infectiologie, Inserm U1111, CNRS UMR5308, École Normale Supérieure de Lyon, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.
Romain ParentCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Serge AdnotINSERM U955, Département de Physiologie - Explorations fonctionnelles, Hôpital Henri Mondor, AP-HP, FHU SENEC, Créteil, France.
Philippe BertolinoCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
Jennifer RieussetCarMeN Laboratory, UMR INSERM U1060/INRA U1397, Lyon 1 University, Pierre bénite, France.
Antonin TortereauVetAgro Sup, Interactions Cellules Environnement (ICE), Université de Lyon, Marcy l'Etoile, France.
David VindrieuxCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.
David BernardCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Lyon, France.ORCID 0000-0002-1557-2074
Université Claude Bernard Lyon 1 · FRInserm · FRHospices Civils de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of senescent cells promotes many age-related alterations and diseases. In this study, we investigated the role of the pro-senescent phospholipase A2 receptor 1 (PLA2R1) in regulating some age-related alterations in old mice and in mice subjected to a Western diet, whereas aged wild-type mice displayed a decreased ability to regulate their glycemia during glucose and insulin tolerance tests, aged Pla2r1 knockout (KO) mice efficiently regulated their glycemia and displayed fewer signs of aging. Loss of Pla2r1 was also found protective against the deleterious effects of a Western diet. Moreover, these Pla2r1 KO mice were partially protected from diet-induced senescent cell accumulation, steatosis, and fibrosis. Together these results support that Pla2r1 drives several age-related alterations, especially in the liver, arising during aging or through a Western diet.

Indexed as

AgingDiet, WesternAnimalsCellular SenescenceMiceMice, KnockoutReceptors, Phospholipase A2Telomere ShorteningPla2r1 protein, mouseReceptors, Phospholipase A2agingcellular senescenceliverWestern diet

Identifiers

PMID37667516
PMCPMC10652324
OpenAlexW4386438545

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.