MicroRNAs in Cardiac Hypertrophy

dc.contributor.authorWehbe, Nadine
dc.contributor.authorNasser, Suzanne A.
dc.contributor.authorPintus, Gianfranco
dc.contributor.authorBadran, Adnan
dc.contributor.authorEid, Ali H.
dc.contributor.authorBaydoun, Elias Abdel Hasan
dc.contributor.departmentDepartment of Biology
dc.contributor.departmentPharmacology and Toxicology
dc.contributor.facultyFaculty of Arts and Sciences (FAS)
dc.contributor.facultyFaculty of Medicine (FM)
dc.contributor.institutionAmerican University of Beirut
dc.date.accessioned2025-01-24T11:20:51Z
dc.date.available2025-01-24T11:20:51Z
dc.date.issued2019
dc.description.abstractLike other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
dc.identifier.doihttps://doi.org/10.3390/ijms20194714
dc.identifier.eid2-s2.0-85072572494
dc.identifier.pmid31547607
dc.identifier.urihttp://hdl.handle.net/10938/25151
dc.language.isoen
dc.publisherMDPI AG
dc.relation.ispartofInternational Journal of Molecular Sciences
dc.sourceScopus
dc.subjectCardiac hypertrophy
dc.subjectCardiac remodeling
dc.subjectCardiomyocytez
dc.subjectMicrornas
dc.subjectTherapeutic targets
dc.subjectAnimals
dc.subjectCardiomegaly
dc.subjectHeart failure
dc.subjectHumans
dc.subjectSignal transduction
dc.subjectCyclin d2
dc.subjectDiacylglycerol
dc.subjectMicrorna
dc.subjectMicrorna 1
dc.subjectMicrorna 10a
dc.subjectMicrorna 124
dc.subjectMicrorna 125b
dc.subjectMicrorna 133
dc.subjectMicrorna 139
dc.subjectMicrorna 15
dc.subjectMicrorna 150
dc.subjectMicrorna 16
dc.subjectMicrorna 19
dc.subjectMicrorna 195
dc.subjectMicrorna 200c
dc.subjectMicrorna 206
dc.subjectMicrorna 208a
dc.subjectMicrorna 23
dc.subjectMicrorna 24
dc.subjectMicrorna 29
dc.subjectMicrorna 297
dc.subjectMicrorna 320
dc.subjectMicrorna 499
dc.subjectMicrorna 590
dc.subjectMitogen activated protein kinase
dc.subjectSerum response factor
dc.subjectSmall interfering rna
dc.subjectStat3 protein
dc.subjectSuppressor of cytokine signaling 1
dc.subjectTranscription factor
dc.subjectUnclassified drug
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectCardiac muscle cell
dc.subjectCell cycle progression
dc.subjectCell division
dc.subjectCell proliferation
dc.subjectDna methylation
dc.subjectDna recombination
dc.subjectDown regulation
dc.subjectEndoplasmic reticulum stress
dc.subjectGene overexpression
dc.subjectGenetic transcription
dc.subjectHeart ventricle hypertrophy
dc.subjectHuman
dc.subjectMrna expression level
dc.subjectMuscle contractility
dc.subjectNonhuman
dc.subjectProtein expression
dc.subjectReview
dc.subjectTranscription regulation
dc.subjectUpregulation
dc.subjectAnimal
dc.subjectMetabolism
dc.subjectPathology
dc.titleMicroRNAs in Cardiac Hypertrophy
dc.typeReview

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