期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1867, 期 10, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.bbadis.2021.166208
关键词
Heart failure with preserved ejection fraction; Mitochondrial metabolism; Mitochondrial dynamics; Mitophagy
资金
- Agencia Nacional de Investigaci 'on y Desarrollo (ANID), Chile: FONDAP [15130011]
- Agencia Nacional de Investigaci 'on y Desarrollo (ANID), Chile: FONDECYT [11190756, 1181097, 1190743, 1211270]
- Proyecto Puente [016-2019]
- Programa de Investigacion Asociativa (PIA)-CONICYT [172066]
- International Centre for Genetic Engineering and Biotechnology (ICGEB) [CRP/CHL18-04]
- University of Chile grant U-Redes Generacion [VID G_201835]
Heart failure is a major cause of hospitalization and mortality worldwide. HFpEF predominantly affects the elderly population with overlapping comorbidities, making diagnosis challenging. Despite extensive research, there is still no evidence-based therapy for HFpEF.
Y 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.
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