Evidence map›Paper›PMID 37708026›Full record

ArticleCell reports2023

CD44 correlates with longevity and enhances basal ATF6 activity and ER stress resistance.

Masaki Takasugi, Naoko Ohtani, Kazuaki Takemura, Stephan Emmrich, Frances T Zakusilo, Yuya Yoshida, Nobuyuki Kutsukake, John N Mariani, Martha S Windrem, Devin Chandler-Militello and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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  7. 1-L Transcription in Prion Diseases.International journal of molecular sciences · 2024
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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

15 authors at 6 institutions in 2 countries.

Masaki TakasugiDepartment of Biology, University of Rochester, Rochester, NY 14627, USA; Department of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan. Electronic address: masaki.takasugi@omu.ac.jp.
Naoko OhtaniDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan. Electronic address: naoko.ohtani@omu.ac.jp.
Kazuaki TakemuraDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Stephan EmmrichDepartment of Biology, University of Rochester, Rochester, NY 14627, USA.
Frances T ZakusiloDepartment of Biology, University of Rochester, Rochester, NY 14627, USA.
Yuya YoshidaDepartment of Pathophysiology, Osaka Metropolitan University, Graduate School of Medicine, Osaka, Japan.
Nobuyuki KutsukakeResearch Center for Integrative Evolutionary Science, SOKENDAI, The Graduate University for Advanced Studies, Kanagawa, Japan.
John N MarianiCenter for Translational Neuromedicine and the Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Martha S WindremCenter for Translational Neuromedicine and the Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Devin Chandler-MilitelloCenter for Translational Neuromedicine and the Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Steven A GoldmanCenter for Translational Neuromedicine and the Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Junko SatohMedical Research Support Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shinji ItoMedical Research Support Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Andrei SeluanovDepartment of Biology, University of Rochester, Rochester, NY 14627, USA; Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642 USA. Electronic address: andrei.seluanov@rochester.edu.
Vera GorbunovaDepartment of Biology, University of Rochester, Rochester, NY 14627, USA; Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642 USA. Electronic address: vera.gorbunova@rochester.edu.
University of Rochester Medical Center · USOsaka Metropolitan University · JPKyoto University · JPUniversity of Rochester · USOsaka Ohtani University · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

The role of hyaluronan in longevity and cancer resistance of longest-lived rodentP01AG047200 · NIA · UNIVERSITY OF ROCHESTER · PI Vadim N. Gladyshev · 2014 to 2026
$36.9M
Somatic Activation of Retrotransposition: A New Molecular Mechanism of Aging?P01AG051449 · NIA · BROWN UNIVERSITY · PI John M Sedivy · 2016 to 2026
$30.4M
Regulation of epigenome stability by SIRT6 during aging. Supplement: Does centenarian variant of SIRT6 or bowhead whale SIRT6 confer protection from Alzheimer's disease?R37AG046320 · NIA · UNIVERSITY OF ROCHESTER · PI Andrei Seluanov · 2019 to 2026
$4.7M
Cell-intrinsic and contextual determinants of aging by human glial progenitor cellsR01AG072298 · NIA · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN · 2021 to 2025
$1.6M
NIA NIH HHS P01 AG047200NIA NIH HHS P01 AG051449NIA NIH HHS R01 AG072298NIA NIH HHS R37 AG046320
6 · The paper itself

Abstract

The naked mole rat (NMR) is the longest-lived rodent, resistant to multiple age-related diseases including neurodegeneration. However, the mechanisms underlying the NMR's resistance to neurodegenerative diseases remain elusive. Here, we isolated oligodendrocyte progenitor cells (OPCs) from NMRs and compared their transcriptome with that of other mammals. Extracellular matrix (ECM) genes best distinguish OPCs of long- and short-lived species. Notably, expression levels of CD44, an ECM-binding protein that has been suggested to contribute to NMR longevity by mediating the effect of hyaluronan (HA), are not only high in OPCs of long-lived species but also positively correlate with longevity in multiple cell types/tissues. We found that CD44 localizes to the endoplasmic reticulum (ER) and enhances basal ATF6 activity. CD44 modifies proteome and membrane properties of the ER and enhances ER stress resistance in a manner dependent on unfolded protein response regulators without the requirement of HA. HA-independent role of CD44 in proteostasis regulation may contribute to mammalian longevity.

Indexed as

Endoplasmic Reticulum StressLongevityAnimalsMole RatsTranscriptomeUnfolded Protein ResponseATF6CD44comparative transcriptomicsCP: Cell biologylongevitynaked mole ratproteostasis

Identifiers

PMID37708026
PMCPMC10591879
OpenAlexW4386700228

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.