Mitochondrial function, dynamics and quality control in the pathophysiology of HFpEF

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dc.contributor.authordel Campo A.
dc.contributor.authorPerez G.
dc.contributor.authorCastro P.F.
dc.contributor.authorVerdejo H.E.
dc.contributor.authorParra V.
dc.contributor.authorParra V.
dc.contributor.authorParra V.
dc.contributor.authorCastro P.F.
dc.contributor.authorParra V.
dc.contributor.authorVerdejo H.E.
dc.date.accessioned2024-01-10T14:23:32Z
dc.date.available2024-01-10T14:23:32Z
dc.date.issued2021
dc.description.abstract© 2021 Elsevier B.V.Heart failure (HF) is one of the leading causes of hospitalization for the adult population and a major cause of mortality worldwide. The HF syndrome is characterized by the heart's inability to supply the cardiac output required to meet the body's metabolic requirements or only at the expense of elevated filling pressures. HF without overt impairment of left ventricular ejection fraction (LVEF) was initially labeled as “diastolic HF” until recognizing the coexistence of both systolic and diastolic abnormalities in most cases. Acknowledging these findings, the preferred nomenclature is HF with preserved EF (HFpEF). This syndrome primarily affects the elderly population and is associated with a heterogeneous overlapping of comorbidities that makes its diagnosis challenging. Despite extensive research, there is still no evidence-based therapy for HFpEF, reinforcing the need for a thorough understanding of the pathophysiology underlying its onset and progression. The role of mitochondrial dysfunction in developing the pathophysiological changes that accompany HFpEF onset and progression (low-grade systemic inflammation, oxidative stress, endothelial dysfunction, and myocardial remodeling) has just begun to be acknowledged. This review summarizes our current understanding of the participation of the mitochondrial network in the pathogenesis of HFpEF, with particular emphasis on the signaling pathways involved, which may provide future therapeutic targets.
dc.description.funderAgencia Nacional de Investigaci?n y Desarrollo
dc.description.funderAgencia Nacional de Investigación y Desarrollo
dc.description.funderInternational Centre for Genetic Engineering and Biotechnology
dc.description.funderCONICYT
dc.description.funderFONDECYT
dc.description.funderUniversity of Chile
dc.description.funderFONDAP
dc.fechaingreso.objetodigital19-04-2024
dc.fuente.origenScopus
dc.identifier.doi10.1016/j.bbadis.2021.166208
dc.identifier.eissn1879260X
dc.identifier.issn1879260X 09254439
dc.identifier.pubmedid34214606
dc.identifier.scopusidSCOPUS_ID:85109434144
dc.identifier.urihttps://doi.org/10.1016/j.bbadis.2021.166208
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/80109
dc.information.autorucFacultad de Medicina; Verdejo Pinochet, Hugo Eduardo; S/I; 1001175
dc.issue.numero166208
dc.language.isoen
dc.nota.accesocontenido parcial
dc.publisherElsevier B.V.
dc.revistaBiochimica et Biophysica Acta - Molecular Basis of Disease
dc.rightsacceso restringido
dc.subjectHeart failure with preserved ejection fraction
dc.subjectMitochondrial dynamics
dc.subjectMitochondrial metabolism
dc.subjectMitophagy
dc.titleMitochondrial function, dynamics and quality control in the pathophysiology of HFpEF
dc.typeartículo de revisión
dc.volumen1867
sipa.codpersvinculados1001175
sipa.indexScopus
sipa.indexPubmed
sipa.trazabilidadCarga SIPA;09-01-2024
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