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RESEARCH PRODUCT
MicroRNA and receptor mediated signaling pathways as potential therapeutic targets in heart failure.
Irene SimonettaAntonino TuttolomondoAntonio Pintosubject
0301 basic medicineheart failure target micro-RNA receptorSettore MED/09 - Medicina InternaClinical BiochemistryCellApoptosisBiology03 medical and health scienceschemistry.chemical_compoundGSK-3Drug DiscoverymicroRNAmedicineAnimalsHumansMyocytes CardiacAntagomirMolecular Targeted TherapyReceptorHeart FailurePharmacologyVentricular RemodelingReceptor-mediated endocytosisCell biologyMicroRNAs030104 developmental biologymedicine.anatomical_structurechemistryImmunologyMolecular MedicineSignal transductionSignal TransductionRelaxin receptordescription
Cardiac remodelling is a complex pathogenetic pathway involving genome expression, molecular, cellular, and interstitial changes that cause changes in size, shape and function of the heart after cardiac injury. Areas covered: We will review recent advances in understanding the role of several receptor-mediated signaling pathways and micro-RNAs, in addition to their potential as candidate target pathways in the pathogenesis of heart failure. The myocyte is the main target cell involved in the remodelling process via ischemia, cell necrosis and apoptosis (by means of various receptor pathways), and other mechanisms mediated by micro-RNAs. We will analyze the role of some receptor mediated signaling pathways such as natriuretic peptides, mediators of glycogen synthase kinase 3 and ERK1/2 pathways, beta-adrenergic receptor subtypes and relaxin receptor signaling mechanisms, TNF/TNF receptor family and TWEAK/Fn14 axis, and some micro-RNAs as candidate target pathways in pathogenesis of heart failure. These mediators of receptor-mediated pathways and micro-RNA are the most addressed targets of emerging therapies in modern heart failure treatment strategies. Expert opinion: Future treatment strategies should address mediators involved in multiple steps within heart failure pathogenetic pathways.
year | journal | country | edition | language |
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2016-07-25 |