2026-04-30T10:43:39Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/188612024-11-29T16:55:17Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Blasco, MA
author
Martinez Rodriguez, Paula
funder
Ministerio de Economía y Competitividad (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Fundación Banco Santander
2024-02-28T10:40:17Z
2024-02-28T10:40:17Z
2018-09-14
Circ Res . 2018 ;123(7):787-802
10.1161/CIRCRESAHA.118.312202
1524-4571
Circulation research
30355079
http://hdl.handle.net/20.500.12105/18861
Telomeres, the protective ends of linear chromosomes, shorten throughout an individual's lifetime. Accumulation of critically short telomeres is proposed to be a primary molecular cause of aging and age-associated diseases. Mutations in telomere maintenance genes are associated with pathologies referred to as or telomeropathies. The rate of telomere shortening throughout life is determined by endogenous (genetic) and external (nongenetic) factors. Therapeutic strategies based on telomerase activation are being developed to treat and prevent telomere-associated diseases, namely aging-related diseases and telomeropathies. Here, we review the molecular mechanisms underlying telomere driven diseases with particular emphasis on cardiovascular diseases.
eng
Heart-Breaking Telomeres.
journal article
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URL
https://repisalud.isciii.es/bitstreams/9de65556-cfa2-4962-9a87-a246f9a3f715/download
File
MD5
45805b1ff3cea9e4a310153b6f4bd24e
2939887
application/pdf
HeartBreakingTelomeres_2018.pdf
URL
https://repisalud.isciii.es/bitstreams/42b9b0f5-4f14-43cf-82d6-1cce134473ce/download
File
MD5
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103367
text/plain
HeartBreakingTelomeres_2018.pdf.txt