New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review

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dc.article.number4407
dc.catalogadordfo
dc.contributor.authorJalil Milad, Jorge Emilio
dc.contributor.authorGabrielli Nervi, Luigi Arnaldo
dc.contributor.authorOcaranza Jeraldino, María Paz
dc.contributor.authorMacNab, P.
dc.contributor.authorFernandez R.
dc.contributor.authorGrassi Corrales, Bruno
dc.contributor.authorJofré Mendoza, Paulina Eugenia
dc.contributor.authorVerdejo, H.
dc.contributor.authorAcevedo, M.
dc.contributor.authorCordova Alvestegui, Samuel Edmundo
dc.contributor.authorSanhueza, Luis
dc.contributor.authorGreig Undurraga, Douglas Patrick
dc.date.accessioned2025-08-27T13:15:47Z
dc.date.available2025-08-27T13:15:47Z
dc.date.issued2024
dc.description.abstractThis review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.
dc.fechaingreso.objetodigital2025-08-27
dc.format.extent24 páginas
dc.fuente.origenSCOPUS
dc.fuente.origenORCID
dc.identifier.doi10.3390/ijms25084407
dc.identifier.issn1661-6596
dc.identifier.scopusidSCOPUS_ID:85191472147
dc.identifier.urihttps://doi.org/10.3390/ijms25084407
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/105299
dc.identifier.wosidWOS:001210719300001
dc.information.autorucEscuela de Medicina; Verdejo Pinochet, Hugo Eduardo; 0000-0003-0078-4792; 1001175
dc.information.autorucEscuela de Medicina; Acevedo Blanco, Monica Andrea; S/I; 81173
dc.information.autorucFacultad de Comunicaciones; Sanhueza Acuna, Luis Manuel; S/I; 175082
dc.information.autorucEscuela de Medicina; Jalil Milad Jorge Emilio; 0000-0001-6877-2072; 99946
dc.information.autorucEscuela de Medicina; Gabrielli Nervi Luigi Arnaldo; 0000-0002-1551-7147; 11086
dc.information.autorucEscuela de Medicina; Ocaranza Jeraldino Maria Paz; 0000-0002-4915-6378; 1001254
dc.information.autorucEscuela de Medicina; Grassi Corrales Bruno; 0000-0003-0095-9740; 132804
dc.information.autorucEscuela de Medicina; Jofre Mendoza Paulina Eugenia; S/I; 1023810
dc.information.autorucEscuela de Medicina; Cordova Alvestegui Samuel Edmundo; S/I; 96819
dc.information.autorucEscuela de Medicina; Greig Undurraga Douglas Patrick; S/I; 15418
dc.issue.numero4407
dc.language.isoen
dc.nota.accesocontenido completo
dc.revistaInternational Journal of Molecular Sciences
dc.rightsacceso abierto
dc.rights.licenseAtribución/Reconocimiento 4.0 Internacional
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectAldosterone
dc.subjectAMPK
dc.subjectDiabetes
dc.subjectGLP-1
dc.subjectHeart failure
dc.subjectHFpEF
dc.subjectMicroinflammation
dc.subjectObesity
dc.subjectPericardial adipose tissue
dc.subjectRemodeling
dc.subjectRenin angiotensin system
dc.subjectRho kinase
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods04 Quality education
dc.subject.odspa04 Educación de calidad
dc.titleNew Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review
dc.typeartículo
dc.volumen25
sipa.codpersvinculados1001175
sipa.codpersvinculados81173
sipa.codpersvinculados175082
sipa.codpersvinculados99946
sipa.codpersvinculados11086
sipa.codpersvinculados1001254
sipa.codpersvinculados132804
sipa.codpersvinculados1023810
sipa.codpersvinculados96819
sipa.codpersvinculados15418
sipa.trazabilidadSCOPUS;2024-05-05
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