Aging and rejuvenation - a modular epigenome model
- Autores
- Chiavellini, Priscila; Canatelli Mallat, Martina; Lehmann, Marianne; Gallardo, María Emilia; Hereñú, Claudia B.; Cordeiro, José L.; Clement, James P.; Goya, Rodolfo Gustavo
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The view of aging has evolved in parallel with the advances in biomedical sciences. Long considered as an irreversible process where interventions were only aimed at slowing down its progression, breakthrough discoveries like animal cloning and cell reprogramming have deeply changed our understanding of postnatal development, giving rise to the emerging view that the epigenome is the driver of aging. The idea was significantly strengthened by the converging discovery that DNA methylation (DNAm) at specific CpG sites could be used as a highly accurate biomarker of age defined by an algorithm known as the Horvath clock. It was at this point where epigenetic rejuvenation came into play as a strategy to reveal to what extent biological age can be set back by making the clock tick backwards. Initial evidence suggests that when the clock is forced to tick backwards in vivo, it is only able to drag the phenotype to a partially rejuvenated condition. In order to explain the results, a bimodular epigenome is proposed, where module A represents the DNAm clock component and module B the remainder of the epigenome. Epigenetic rejuvenation seems to hold the key to arresting or even reversing organismal aging.
Instituto de Investigaciones Bioquímicas de La Plata - Materia
-
Bioquímica
Aging
DNA methylation
Epigenetic clock
Rejuvenation
Cell reprogramming - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/3.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/128713
Ver los metadatos del registro completo
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Aging and rejuvenation - a modular epigenome modelChiavellini, PriscilaCanatelli Mallat, MartinaLehmann, MarianneGallardo, María EmiliaHereñú, Claudia B.Cordeiro, José L.Clement, James P.Goya, Rodolfo GustavoBioquímicaAgingDNA methylationEpigenetic clockRejuvenationCell reprogrammingThe view of aging has evolved in parallel with the advances in biomedical sciences. Long considered as an irreversible process where interventions were only aimed at slowing down its progression, breakthrough discoveries like animal cloning and cell reprogramming have deeply changed our understanding of postnatal development, giving rise to the emerging view that the epigenome is the driver of aging. The idea was significantly strengthened by the converging discovery that DNA methylation (DNAm) at specific CpG sites could be used as a highly accurate biomarker of age defined by an algorithm known as the Horvath clock. It was at this point where epigenetic rejuvenation came into play as a strategy to reveal to what extent biological age can be set back by making the clock tick backwards. Initial evidence suggests that when the clock is forced to tick backwards in vivo, it is only able to drag the phenotype to a partially rejuvenated condition. In order to explain the results, a bimodular epigenome is proposed, where module A represents the DNAm clock component and module B the remainder of the epigenome. Epigenetic rejuvenation seems to hold the key to arresting or even reversing organismal aging.Instituto de Investigaciones Bioquímicas de La Plata2021info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf4734-4746http://sedici.unlp.edu.ar/handle/10915/128713enginfo:eu-repo/semantics/altIdentifier/issn/1945-4589info:eu-repo/semantics/altIdentifier/pmid/33627519info:eu-repo/semantics/altIdentifier/doi/10.18632/aging.202712info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/3.0/Creative Commons Attribution 3.0 Unported (CC BY 3.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-17T10:13:42Zoai:sedici.unlp.edu.ar:10915/128713Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-17 10:13:42.704SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Aging and rejuvenation - a modular epigenome model |
title |
Aging and rejuvenation - a modular epigenome model |
spellingShingle |
Aging and rejuvenation - a modular epigenome model Chiavellini, Priscila Bioquímica Aging DNA methylation Epigenetic clock Rejuvenation Cell reprogramming |
title_short |
Aging and rejuvenation - a modular epigenome model |
title_full |
Aging and rejuvenation - a modular epigenome model |
title_fullStr |
Aging and rejuvenation - a modular epigenome model |
title_full_unstemmed |
Aging and rejuvenation - a modular epigenome model |
title_sort |
Aging and rejuvenation - a modular epigenome model |
dc.creator.none.fl_str_mv |
Chiavellini, Priscila Canatelli Mallat, Martina Lehmann, Marianne Gallardo, María Emilia Hereñú, Claudia B. Cordeiro, José L. Clement, James P. Goya, Rodolfo Gustavo |
author |
Chiavellini, Priscila |
author_facet |
Chiavellini, Priscila Canatelli Mallat, Martina Lehmann, Marianne Gallardo, María Emilia Hereñú, Claudia B. Cordeiro, José L. Clement, James P. Goya, Rodolfo Gustavo |
author_role |
author |
author2 |
Canatelli Mallat, Martina Lehmann, Marianne Gallardo, María Emilia Hereñú, Claudia B. Cordeiro, José L. Clement, James P. Goya, Rodolfo Gustavo |
author2_role |
author author author author author author author |
dc.subject.none.fl_str_mv |
Bioquímica Aging DNA methylation Epigenetic clock Rejuvenation Cell reprogramming |
topic |
Bioquímica Aging DNA methylation Epigenetic clock Rejuvenation Cell reprogramming |
dc.description.none.fl_txt_mv |
The view of aging has evolved in parallel with the advances in biomedical sciences. Long considered as an irreversible process where interventions were only aimed at slowing down its progression, breakthrough discoveries like animal cloning and cell reprogramming have deeply changed our understanding of postnatal development, giving rise to the emerging view that the epigenome is the driver of aging. The idea was significantly strengthened by the converging discovery that DNA methylation (DNAm) at specific CpG sites could be used as a highly accurate biomarker of age defined by an algorithm known as the Horvath clock. It was at this point where epigenetic rejuvenation came into play as a strategy to reveal to what extent biological age can be set back by making the clock tick backwards. Initial evidence suggests that when the clock is forced to tick backwards in vivo, it is only able to drag the phenotype to a partially rejuvenated condition. In order to explain the results, a bimodular epigenome is proposed, where module A represents the DNAm clock component and module B the remainder of the epigenome. Epigenetic rejuvenation seems to hold the key to arresting or even reversing organismal aging. Instituto de Investigaciones Bioquímicas de La Plata |
description |
The view of aging has evolved in parallel with the advances in biomedical sciences. Long considered as an irreversible process where interventions were only aimed at slowing down its progression, breakthrough discoveries like animal cloning and cell reprogramming have deeply changed our understanding of postnatal development, giving rise to the emerging view that the epigenome is the driver of aging. The idea was significantly strengthened by the converging discovery that DNA methylation (DNAm) at specific CpG sites could be used as a highly accurate biomarker of age defined by an algorithm known as the Horvath clock. It was at this point where epigenetic rejuvenation came into play as a strategy to reveal to what extent biological age can be set back by making the clock tick backwards. Initial evidence suggests that when the clock is forced to tick backwards in vivo, it is only able to drag the phenotype to a partially rejuvenated condition. In order to explain the results, a bimodular epigenome is proposed, where module A represents the DNAm clock component and module B the remainder of the epigenome. Epigenetic rejuvenation seems to hold the key to arresting or even reversing organismal aging. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://sedici.unlp.edu.ar/handle/10915/128713 |
url |
http://sedici.unlp.edu.ar/handle/10915/128713 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/issn/1945-4589 info:eu-repo/semantics/altIdentifier/pmid/33627519 info:eu-repo/semantics/altIdentifier/doi/10.18632/aging.202712 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/3.0/ Creative Commons Attribution 3.0 Unported (CC BY 3.0) |
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openAccess |
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http://creativecommons.org/licenses/by/3.0/ Creative Commons Attribution 3.0 Unported (CC BY 3.0) |
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application/pdf 4734-4746 |
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SEDICI (UNLP) - Universidad Nacional de La Plata |
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