Evidence map›Paper›PMID 31980643›Full record

ArticleNature communications2020

Endothelial progeria induces adipose tissue senescence and impairs insulin sensitivity through senescence associated secretory phenotype.

Agian Jeffilano Barinda, Koji Ikeda, Dhite Bayu Nugroho, Donytra Arby Wardhana, Naoto Sasaki, Sakiko Honda, Ryota Urata, Satoaki Matoba, Ken-Ichi Hirata, Noriaki Emoto

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 104 citations in OpenAlex.

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  9. Matrix stiffness induces endothelial network senescence.bioRxiv : the preprint server for biology · 2025
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  20. Frontiers in endocrinology · 2025
    Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Agian Jeffilano BarindaLaboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan.ORCID http://orcid.org/0000-0002-5864-3725
Koji IkedaLaboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan. ikedak-circ@umin.ac.jp.
Dhite Bayu NugrohoLaboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan.ORCID http://orcid.org/0000-0003-2483-9970
Donytra Arby WardhanaLaboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan.
Naoto SasakiLaboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan.
Sakiko HondaDepartment of Cardiology, Kyoto Prefectural University Graduate School of Medical Science, 465 Kajii, Kawaramachi-Hirokoji, Kyoto, 602-8566, Japan.
Ryota UrataDepartment of Cardiology, Kyoto Prefectural University Graduate School of Medical Science, 465 Kajii, Kawaramachi-Hirokoji, Kyoto, 602-8566, Japan.
Satoaki MatobaDepartment of Cardiology, Kyoto Prefectural University Graduate School of Medical Science, 465 Kajii, Kawaramachi-Hirokoji, Kyoto, 602-8566, Japan.
Ken-Ichi HirataDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki, Chuo, Kobe, 6500017, Japan.
Noriaki EmotoLaboratory of Clinical Pharmaceutical Science, Kobe Pharmaceutical University, 4-19-1 Motoyamakitamachi, Higashinada, Kobe, 658-8558, Japan.
Kobe Pharmaceutical University · JPKyoto Prefectural University of Medicine · JPKobe University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular senescence is thought to play a crucial role in an ageing-associated decline of organ functions; however, whether vascular senescence is causally implicated in age-related disease remains unclear. Here we show that endothelial cell (EC) senescence induces metabolic disorders through the senescence-associated secretory phenotype. Senescence-messaging secretomes from senescent ECs induced a senescence-like state and reduced insulin receptor substrate-1 in adipocytes, which thereby impaired insulin signaling. We generated EC-specific progeroid mice that overexpressed the dominant negative form of telomeric repeat-binding factor 2 under the control of the Tie2 promoter. EC-specific progeria impaired systemic metabolic health in mice in association with adipose tissue dysfunction even while consuming normal chow. Notably, shared circulation with EC-specific progeroid mice by parabiosis sufficiently transmitted the metabolic disorders into wild-type recipient mice. Our data provides direct evidence that EC senescence impairs systemic metabolic health, and thus establishes EC senescence as a bona fide risk for age-related metabolic disease.

Indexed as

Cellular SenescenceInsulin ResistanceAdipocytes, WhiteAdipose Tissue, WhiteAnimalsDisease Models, AnimalEndothelial CellsInterleukin-1alphaMiceMice, TransgenicOxidative StressProgeriaPromoter Regions, GeneticReceptor, TIE-2Signal TransductionTelomeric Repeat Binding Protein 2Interleukin-1alphaReceptor, TIE-2Tek protein, mouseTelomeric Repeat Binding Protein 2

Identifiers

PMID31980643
PMCPMC6981212
OpenAlexW3002038471

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.