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Cardiomyocyte Telomere Damage by ROS without Cell Division


ABSTRACT: N/A

SUBMITTER: Carole Proctor 

PROVIDER: MODEL1608250001 | biostudies-other |

SECONDARY ACCESSION(S): 30737259

REPOSITORIES: biostudies-other

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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   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]

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