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- Publisher Website: 10.1042/CS20110115
- Scopus: eid_2-s2.0-80052316167
- PMID: 21699498
- WOS: WOS:000296120400005
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Article: Molecular mechanisms of cardiomyocyte aging
Title | Molecular mechanisms of cardiomyocyte aging |
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Authors | |
Keywords | Aging Apoptosis Cardiomyocyte Cardiovascular Disease. |
Issue Date | 2011 |
Citation | Clinical Science, 2011, v. 121 n. 8, p. 315-329 How to Cite? |
Abstract | Western societies are rapidly aging, and cardiovascular diseases are the leading cause of death. In fact, age and cardiovascular diseases are positively correlated, and disease syndromes affecting the heart reach epidemic proportions in the very old. Genetic variations and molecular adaptations are the primary contributors to the onset of cardiovascular disease; however, molecular links between age and heart syndromes are complex and involve much more than the passage of time. Changes in CM (cardiomyocyte) structure and function occur with age and precede anatomical and functional changes in the heart. Concomitant with or preceding some of these cellular changes are alterations in gene expression often linked to signalling cascades that may lead to a loss of CMs or reduced function. An understanding of the intrinsic molecular mechanisms underlying these cascading events has been instrumental in forming our current understanding of how CMs adapt with age. In the present review, we describe the molecular mechanisms underlying CM aging and how these changes may contribute to the development of cardiovascular diseases. © The Authors Journal compilation © 2011 Biochemical Society. |
Persistent Identifier | http://hdl.handle.net/10722/195140 |
ISSN | 2023 Impact Factor: 6.7 2023 SCImago Journal Rankings: 1.565 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Anna, A | - |
dc.contributor.author | Riordon, DR | - |
dc.contributor.author | Boheler, KR | - |
dc.date.accessioned | 2014-02-25T01:40:13Z | - |
dc.date.available | 2014-02-25T01:40:13Z | - |
dc.date.issued | 2011 | - |
dc.identifier.citation | Clinical Science, 2011, v. 121 n. 8, p. 315-329 | - |
dc.identifier.issn | 0143-5221 | - |
dc.identifier.uri | http://hdl.handle.net/10722/195140 | - |
dc.description.abstract | Western societies are rapidly aging, and cardiovascular diseases are the leading cause of death. In fact, age and cardiovascular diseases are positively correlated, and disease syndromes affecting the heart reach epidemic proportions in the very old. Genetic variations and molecular adaptations are the primary contributors to the onset of cardiovascular disease; however, molecular links between age and heart syndromes are complex and involve much more than the passage of time. Changes in CM (cardiomyocyte) structure and function occur with age and precede anatomical and functional changes in the heart. Concomitant with or preceding some of these cellular changes are alterations in gene expression often linked to signalling cascades that may lead to a loss of CMs or reduced function. An understanding of the intrinsic molecular mechanisms underlying these cascading events has been instrumental in forming our current understanding of how CMs adapt with age. In the present review, we describe the molecular mechanisms underlying CM aging and how these changes may contribute to the development of cardiovascular diseases. © The Authors Journal compilation © 2011 Biochemical Society. | - |
dc.language | eng | - |
dc.relation.ispartof | Clinical Science | - |
dc.subject | Aging | - |
dc.subject | Apoptosis | - |
dc.subject | Cardiomyocyte | - |
dc.subject | Cardiovascular Disease. | - |
dc.title | Molecular mechanisms of cardiomyocyte aging | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1042/CS20110115 | - |
dc.identifier.pmid | 21699498 | - |
dc.identifier.scopus | eid_2-s2.0-80052316167 | - |
dc.identifier.volume | 121 | - |
dc.identifier.issue | 8 | - |
dc.identifier.spage | 315 | - |
dc.identifier.epage | 329 | - |
dc.identifier.isi | WOS:000296120400005 | - |
dc.identifier.issnl | 0143-5221 | - |