Heart failure: advances through genomics

Esther E. Creemers; Arthur A. Wilde; Yigal M. Pinto

doi:https://doi.org/10.1038/nrg2983

Heart failure: advances through genomics

Esther E. Creemers, Arthur A. Wilde, Yigal M. Pinto

Research output: Contribution to journal › Review article › Academic › peer-review

58 Citations (Scopus)

Abstract

Heart failure is an increasingly prevalent and highly lethal disease that is most often caused by underlying pathologies, such as myocardial infarction or hypertension, but it can also be the result of a single gene mutation. Comprehensive genetic and genomic approaches are starting to disentangle the diverse molecular underpinnings of both forms of the disease and promise to yield much-needed novel diagnostic and therapeutic options for specific subtypes of heart failure

Original language	English
Pages (from-to)	357-362
Journal	Nature reviews. Genetics
Volume	12
Issue number	5
DOIs	https://doi.org/10.1038/nrg2983
Publication status	Published - 2011

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https://doi.org/10.1038/nrg2983

Cite this

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abstract = "Heart failure is an increasingly prevalent and highly lethal disease that is most often caused by underlying pathologies, such as myocardial infarction or hypertension, but it can also be the result of a single gene mutation. Comprehensive genetic and genomic approaches are starting to disentangle the diverse molecular underpinnings of both forms of the disease and promise to yield much-needed novel diagnostic and therapeutic options for specific subtypes of heart failure",

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AB - Heart failure is an increasingly prevalent and highly lethal disease that is most often caused by underlying pathologies, such as myocardial infarction or hypertension, but it can also be the result of a single gene mutation. Comprehensive genetic and genomic approaches are starting to disentangle the diverse molecular underpinnings of both forms of the disease and promise to yield much-needed novel diagnostic and therapeutic options for specific subtypes of heart failure

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DO - https://doi.org/10.1038/nrg2983

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