A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF
Heart failure with preserved ejection fraction (HFpEF) is one of the most complex and most prevalent cardiometabolic diseases in aging population. Age, obesity, diabetes, and hypertension are the main comorbidities of HFpEF. Microvascular dysfunction and vascular remodeling play a major role in its...
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| Format: | Article |
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Frontiers Media S.A.
2022-11-01
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| Series: | Frontiers in Endocrinology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2022.1057349/full |
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| author | Fernanda Sanhueza-Olivares Mayarling F. Troncoso Francisco Pino-de la Fuente Javiera Martinez-Bilbao Jaime A. Riquelme Ignacio Norambuena-Soto Monica Villa Sergio Lavandero Sergio Lavandero Pablo F. Castro Mario Chiong |
| author_facet | Fernanda Sanhueza-Olivares Mayarling F. Troncoso Francisco Pino-de la Fuente Javiera Martinez-Bilbao Jaime A. Riquelme Ignacio Norambuena-Soto Monica Villa Sergio Lavandero Sergio Lavandero Pablo F. Castro Mario Chiong |
| author_sort | Fernanda Sanhueza-Olivares |
| collection | DOAJ |
| description | Heart failure with preserved ejection fraction (HFpEF) is one of the most complex and most prevalent cardiometabolic diseases in aging population. Age, obesity, diabetes, and hypertension are the main comorbidities of HFpEF. Microvascular dysfunction and vascular remodeling play a major role in its development. Among the many mechanisms involved in this process, vascular stiffening has been described as one the most prevalent during HFpEF, leading to ventricular-vascular uncoupling and mismatches in aged HFpEF patients. Aged blood vessels display an increased number of senescent endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). This is consistent with the fact that EC and cardiomyocyte cell senescence has been reported during HFpEF. Autophagy plays a major role in VSMCs physiology, regulating phenotypic switch between contractile and synthetic phenotypes. It has also been described that autophagy can regulate arterial stiffening and EC and VSMC senescence. Many studies now support the notion that targeting autophagy would help with the treatment of many cardiovascular and metabolic diseases. In this review, we discuss the mechanisms involved in autophagy-mediated vascular senescence and whether this could be a driver in the development and progression of HFpEF. |
| first_indexed | 2024-04-13T10:34:15Z |
| format | Article |
| id | doaj.art-ba2054dc6fed47969814acdf6a2b16ff |
| institution | Directory Open Access Journal |
| issn | 1664-2392 |
| language | English |
| last_indexed | 2024-04-13T10:34:15Z |
| publishDate | 2022-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj.art-ba2054dc6fed47969814acdf6a2b16ff2022-12-22T02:50:06ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922022-11-011310.3389/fendo.2022.10573491057349A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEFFernanda Sanhueza-Olivares0Mayarling F. Troncoso1Francisco Pino-de la Fuente2Javiera Martinez-Bilbao3Jaime A. Riquelme4Ignacio Norambuena-Soto5Monica Villa6Sergio Lavandero7Sergio Lavandero8Pablo F. Castro9Mario Chiong10Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileDivision of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United StatesAdvanced Center for Chronic Diseases, Faculty of Medicine, Pontifical University Catholic of Chile, Santiago, ChileAdvanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santiago, ChileHeart failure with preserved ejection fraction (HFpEF) is one of the most complex and most prevalent cardiometabolic diseases in aging population. Age, obesity, diabetes, and hypertension are the main comorbidities of HFpEF. Microvascular dysfunction and vascular remodeling play a major role in its development. Among the many mechanisms involved in this process, vascular stiffening has been described as one the most prevalent during HFpEF, leading to ventricular-vascular uncoupling and mismatches in aged HFpEF patients. Aged blood vessels display an increased number of senescent endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). This is consistent with the fact that EC and cardiomyocyte cell senescence has been reported during HFpEF. Autophagy plays a major role in VSMCs physiology, regulating phenotypic switch between contractile and synthetic phenotypes. It has also been described that autophagy can regulate arterial stiffening and EC and VSMC senescence. Many studies now support the notion that targeting autophagy would help with the treatment of many cardiovascular and metabolic diseases. In this review, we discuss the mechanisms involved in autophagy-mediated vascular senescence and whether this could be a driver in the development and progression of HFpEF.https://www.frontiersin.org/articles/10.3389/fendo.2022.1057349/fullautophagyHFpEF - heart failure with preserved ejection fractionvascular senescencevascular agingobesitydiabetes |
| spellingShingle | Fernanda Sanhueza-Olivares Mayarling F. Troncoso Francisco Pino-de la Fuente Javiera Martinez-Bilbao Jaime A. Riquelme Ignacio Norambuena-Soto Monica Villa Sergio Lavandero Sergio Lavandero Pablo F. Castro Mario Chiong A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF Frontiers in Endocrinology autophagy HFpEF - heart failure with preserved ejection fraction vascular senescence vascular aging obesity diabetes |
| title | A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF |
| title_full | A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF |
| title_fullStr | A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF |
| title_full_unstemmed | A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF |
| title_short | A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF |
| title_sort | potential role of autophagy mediated vascular senescence in the pathophysiology of hfpef |
| topic | autophagy HFpEF - heart failure with preserved ejection fraction vascular senescence vascular aging obesity diabetes |
| url | https://www.frontiersin.org/articles/10.3389/fendo.2022.1057349/full |
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