Dataset Information

Cardiomyocyte Telomere Damage

ABSTRACT: No description

SUBMITTER: Carole Proctor

PROVIDER: MODEL1608250000 | BioModels | 2019-02-14

REPOSITORIES: BioModels

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			Action	DRS
	MODEL1608250000?filename=MODEL1608250000_url.xml	Xml

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Publications

Length-independent telomere damage drives post-mitotic cardiomyocyte senescence.

Anderson Rhys R Lagnado Anthony A Maggiorani Damien D Walaszczyk Anna A Dookun Emily E Chapman James J Birch Jodie J Salmonowicz Hanna H Ogrodnik Mikolaj M Jurk Diana D Proctor Carole C Correia-Melo Clara C Victorelli Stella S Fielder Edward E Berlinguer-Palmini Rolando R Owens Andrew A Greaves Laura C LC Kolsky Kathy L KL Parini Angelo A Douin-Echinard Victorine V LeBrasseur Nathan K NK Arthur Helen M HM Tual-Chalot Simon S Schafer Marissa J MJ Roos Carolyn M CM Miller Jordan D JD Robertson Neil N Mann Jelena J Adams Peter D PD Tchkonia Tamara T Kirkland James L JL Mialet-Perez Jeanne J Richardson Gavin D GD Passos João F JF

The EMBO journal 20190208 5

Ageing is the biggest risk factor for cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated in age-related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing/post-mitotic cardiomyocytes and investigate whether clearance of senescent cells attenuates age-related cardiac dysfunction. During ageing, human and murine cardiomyocytes acquire a senescent-like phenotype characterised by persistent ...[more]

PMID: 30737259

Dataset Information

Cardiomyocyte Telomere Damage

Dataset's files

Publications

Length-independent telomere damage drives post-mitotic cardiomyocyte senescence.

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