Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms17040502
DC FieldValue
dc.titleMicroRNA and heart failure
dc.contributor.authorWong, L.L
dc.contributor.authorWang, J
dc.contributor.authorLiew, O.W
dc.contributor.authorRichards, A.M
dc.contributor.authorChen, Y.-T
dc.date.accessioned2020-11-10T07:59:15Z
dc.date.available2020-11-10T07:59:15Z
dc.date.issued2016
dc.identifier.citationWong, L.L, Wang, J, Liew, O.W, Richards, A.M, Chen, Y.-T (2016). MicroRNA and heart failure. International Journal of Molecular Sciences 17 (4). ScholarBank@NUS Repository. https://doi.org/10.3390/ijms17040502
dc.identifier.issn16616596
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/183342
dc.description.abstractHeart failure (HF) imposes significant economic and public health burdens upon modern society. It is known that disturbances in neurohormonal status play an important role in the pathogenesis of HF. Therapeutics that antagonize selected neurohormonal pathways, specifically the renin-angiotensin-aldosterone and sympathetic nervous systems, have significantly improved patient outcomes in HF. Nevertheless, mortality remains high with about 50% of HF patients dying within five years of diagnosis thus mandating ongoing efforts to improve HF management. The discovery of short noncoding microRNAs (miRNAs) and our increasing understanding of their functions, has presented potential therapeutic applications in complex diseases, including HF. Results from several genome-wide miRNA studies have identified miRNAs differentially expressed in HF cohorts suggesting their possible involvement in the pathogenesis of HF and their potential as both biomarkers and as therapeutic targets. Unravelling the functional relevance of miRNAs within pathogenic pathways is a major challenge in cardiovascular research. In this article, we provide an overview of the role of miRNAs in the cardiovascular system. We highlight several HF-related miRNAs reported from selected cohorts and review their putative roles in neurohormonal signaling. @ 2016 by the authors; licensee MDPI, Basel, Switzerland.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectcapadenoson
dc.subjectdicer
dc.subjectmicroRNA
dc.subjectmicroRNA 1
dc.subjectmicroRNA 100
dc.subjectmicroRNA 107
dc.subjectmicroRNA 122
dc.subjectmicroRNA 1246
dc.subjectmicroRNA 1254
dc.subjectmicroRNA 126
dc.subjectmicroRNA 133a
dc.subjectmicroRNA 133b
dc.subjectmicroRNA 142 3p
dc.subjectmicroRNA 15
dc.subjectmicroRNA 17
dc.subjectmicroRNA 17 5p
dc.subjectmicroRNA 183 3p
dc.subjectmicroRNA 18a
dc.subjectmicroRNA 195
dc.subjectmicroRNA 208a
dc.subjectmicroRNA 208b
dc.subjectmicroRNA 20a
dc.subjectmicroRNA 499
dc.subjectmicroRNA 92a
dc.subjectmicroRNA 92b
dc.subjectmineralocorticoid antagonist
dc.subjectmyosin heavy chain alpha
dc.subjectneurohormone
dc.subjectspironolactone
dc.subjectunclassified drug
dc.subjectunindexed drug
dc.subjecthormone
dc.subjectmicroRNA
dc.subjectapoptosis
dc.subjectbiogenesis
dc.subjectclinical trial (topic)
dc.subjectgene expression
dc.subjectgene targeting
dc.subjectheart arrhythmia
dc.subjectheart development
dc.subjectheart failure
dc.subjectheart hypertrophy
dc.subjectheart left ventricle ejection fraction
dc.subjecthuman
dc.subjectmulticenter study (topic)
dc.subjectnonhuman
dc.subjectphase 1 clinical trial (topic)
dc.subjectphase 2 clinical trial (topic)
dc.subjectReview
dc.subjectanimal
dc.subjectgenetics
dc.subjectheart failure
dc.subjectmetabolism
dc.subjectsignal transduction
dc.subjectAnimals
dc.subjectHeart Failure
dc.subjectHormones
dc.subjectHumans
dc.subjectMicroRNAs
dc.subjectSignal Transduction
dc.typeReview
dc.contributor.departmentMEDICINE
dc.description.doi10.3390/ijms17040502
dc.description.sourcetitleInternational Journal of Molecular Sciences
dc.description.volume17
dc.description.issue4
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