MicroRNAs in the failing heart - Novel therapeutic targets?
(2014) In Scandinavian Cardiovascular Journal 48(6). p.328-334- Abstract
- Abstract Heart failure is a common and disabling disease with high mortality that carries substantial societal costs. Current therapeutic strategies are aimed at relieving symptoms, avoiding hospitalization, and prolonging life, but disease progression is ultimately inevitable. MicroRNAs (miRNAs) are short, non-coding RNA molecules with pervasive roles in eukaryotic biology, annealing to complimentary sites on target mRNAs, and repressing gene expression. The fact that miRNAs are dysregulated in many human disorders, including cardiovascular disease, and the relative ease with which endogenous miRNA expression can be altered using synthetic antisense oligos has stirred enthusiasm for these molecules as potential drug targets. The aim of... (More)
- Abstract Heart failure is a common and disabling disease with high mortality that carries substantial societal costs. Current therapeutic strategies are aimed at relieving symptoms, avoiding hospitalization, and prolonging life, but disease progression is ultimately inevitable. MicroRNAs (miRNAs) are short, non-coding RNA molecules with pervasive roles in eukaryotic biology, annealing to complimentary sites on target mRNAs, and repressing gene expression. The fact that miRNAs are dysregulated in many human disorders, including cardiovascular disease, and the relative ease with which endogenous miRNA expression can be altered using synthetic antisense oligos has stirred enthusiasm for these molecules as potential drug targets. The aim of this review article was to summarize the current knowledge on the roles of miRNA in the pathophysiology of heart failure as well as the use of miRNAs as therapeutic targets and diagnostic tools for the disease. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4820168
- author
- Gidlöf, Olof
LU
and Erlinge, David
LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scandinavian Cardiovascular Journal
- volume
- 48
- issue
- 6
- pages
- 328 - 334
- publisher
- Taylor & Francis
- external identifiers
-
- pmid:25375881
- wos:000345601200002
- scopus:84913621141
- pmid:25375881
- ISSN
- 1651-2006
- DOI
- 10.3109/14017431.2014.983965
- language
- English
- LU publication?
- yes
- id
- c9b264ae-5d1d-49ae-9211-c720c7839cfe (old id 4820168)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25375881?dopt=Abstract
- date added to LUP
- 2016-04-01 10:09:43
- date last changed
- 2022-03-12 02:44:37
@article{c9b264ae-5d1d-49ae-9211-c720c7839cfe, abstract = {{Abstract Heart failure is a common and disabling disease with high mortality that carries substantial societal costs. Current therapeutic strategies are aimed at relieving symptoms, avoiding hospitalization, and prolonging life, but disease progression is ultimately inevitable. MicroRNAs (miRNAs) are short, non-coding RNA molecules with pervasive roles in eukaryotic biology, annealing to complimentary sites on target mRNAs, and repressing gene expression. The fact that miRNAs are dysregulated in many human disorders, including cardiovascular disease, and the relative ease with which endogenous miRNA expression can be altered using synthetic antisense oligos has stirred enthusiasm for these molecules as potential drug targets. The aim of this review article was to summarize the current knowledge on the roles of miRNA in the pathophysiology of heart failure as well as the use of miRNAs as therapeutic targets and diagnostic tools for the disease.}}, author = {{Gidlöf, Olof and Erlinge, David}}, issn = {{1651-2006}}, language = {{eng}}, number = {{6}}, pages = {{328--334}}, publisher = {{Taylor & Francis}}, series = {{Scandinavian Cardiovascular Journal}}, title = {{MicroRNAs in the failing heart - Novel therapeutic targets?}}, url = {{http://dx.doi.org/10.3109/14017431.2014.983965}}, doi = {{10.3109/14017431.2014.983965}}, volume = {{48}}, year = {{2014}}, }