2021
Loss of hepatic miR-33 improves metabolic homeostasis and liver function without altering body weight or atherosclerosis
Price NL, Zhang X, Fernández-Tussy P, Singh AK, Burnap SA, Rotllan N, Goedeke L, Sun J, Canfrán-Duque A, Aryal B, Mayr M, Suárez Y, Fernández-Hernando C. Loss of hepatic miR-33 improves metabolic homeostasis and liver function without altering body weight or atherosclerosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2006478118. PMID: 33495342, PMCID: PMC7865172, DOI: 10.1073/pnas.2006478118.Peer-Reviewed Original ResearchConceptsMiR-33 deficiencyHDL-C levelsMiR-33Body weightAtherosclerotic plaque sizeAtherosclerotic plaque burdenDevelopment of fibrosisCholesterol transport capacityCholesterol transporter ABCA1High-density lipoprotein biogenesisSREBP2 transcription factorKnockout mouse modelConditional knockout mouse modelPlaque burdenCardiometabolic diseasesChow dietLiver functionMetabolic dysfunctionHDL metabolismHyperlipidemic conditionsMouse modelGlucose homeostasisCholesterol effluxLipid metabolismObesity
2020
Uncovering the Specific Functions of miR-33 in Regulation of Feeding and Cardiometabolic Diseases Linked to Aging
Price N, Zhang X, Fernandez-Tussy P, de Cabo R, Fernandez-Hernando C. Uncovering the Specific Functions of miR-33 in Regulation of Feeding and Cardiometabolic Diseases Linked to Aging. Innovation In Aging 2020, 4: 128-128. PMCID: PMC7741365, DOI: 10.1093/geroni/igaa057.421.Peer-Reviewed Original ResearchMiR-33Cardiometabolic diseasesMetabolic dysfunctionHigh fat diet fed miceFat Diet-Fed MiceMetabolic tissuesDiet fed miceDevelopment of obesityMacrophage cholesterol effluxDevelopment of atherosclerosisRegulation of feedingCholesterol transporter ABCA1Unique mouse modelKey metabolic tissuesDifferent metabolic tissuesFeeding behaviorFed miceHeart diseaseInflammatory responseMouse modelRelated health issuesCholesterol effluxKnockout miceDeficient animalsAtherosclerosis
2018
Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis
Aryal B, Singh AK, Zhang X, Varela L, Rotllan N, Goedeke L, Chaube B, Camporez JP, Vatner DF, Horvath TL, Shulman GI, Suárez Y, Fernández-Hernando C. Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis. JCI Insight 2018, 3: e97918. PMID: 29563332, PMCID: PMC5926923, DOI: 10.1172/jci.insight.97918.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipose TissueAllelesAngiopoietin-Like Protein 4AnimalsAtherosclerosisBody WeightChemokinesCytokinesDiet, High-FatDiet, WesternFatty AcidsGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesGlucoseInsulinIntegrasesIntercellular Signaling Peptides and ProteinsLipid MetabolismLipoprotein LipaseLipoproteinsLiverMaleMiceMice, Inbred C57BLMice, KnockoutMusclesObesityProprotein Convertase 9TriglyceridesConceptsAngiopoietin-like protein 4High-fat dietEctopic lipid depositionLipid depositionGlucose toleranceLipoprotein lipaseShort-term high-fat dietSevere metabolic abnormalitiesProgression of atherosclerosisMajor risk factorTriacylglycerol-rich lipoproteinsFatty acid uptakeAdipose tissue resultsProatherogenic lipoproteinsCardiometabolic diseasesMetabolic abnormalitiesKO miceRisk factorsWhole body lipidMetabolic disordersGlucose metabolismLPL activityAdipose tissueGenetic ablationRapid clearance
2017
Noncoding RNAs in Cholesterol Metabolism and Atherosclerosis
Price N, Fernández-Hernando C. Noncoding RNAs in Cholesterol Metabolism and Atherosclerosis. Cardiac And Vascular Biology 2017, 2: 21-37. DOI: 10.1007/978-3-319-52945-5_2.Peer-Reviewed Original ResearchLow-density lipoprotein cholesterolPlasma LDL-C levelsDysregulation of cholesterolLDL-C levelsPrimary risk factorTreatment of atherosclerosisLipoprotein cholesterolCardiometabolic diseasesCholesterol levelsRisk factorsEffective therapyCholesterol metabolismAtherosclerosisHuman morbidityProper metabolic functionProminent causeElevated levelsLipid homeostasisGenetic factorsDiseaseCholesterolMetabolic functionsMorbidityLevelsPosttranscriptional level