ArticleJournal of the American Heart Association2020
Endothelial Sirtuin 3 Dictates Glucose Transport to Cardiomyocyte and Sensitizes Pressure Overload-Induced Heart Failure.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Sirtuins in Medicine: Multifaceted Roles in Physiological Processes and Cardiovascular Diseases.Biomolecules · 2026Review
- International Union of Basic and Clinical Pharmacology. CXXI. Apelin receptor pharmacology in the human cardiovascular system and emerging clinical applications.Pharmacological reviews · 2026Review
- Cellular Interactions and Immunometabolic Mechanisms in Heart Failure With Preserved Ejection Fraction: From Molecular Mechanisms to Clinical Evidence.Circulation. Heart failure · 2026Review
- Endothelial cell metabolism in cardiovascular physiology and disease.Nature reviews. Cardiology · 2025Review
- Targeting SIRT3 to Ameliorate Diabetic Cardiomyopathy: Progress in Mechanistic Research and Prospects for Clinical Translation.Journal of diabetes · 2025Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025Review
- Emerging interactions between mitochondria and NADTrends in endocrinology and metabolism: TEM · 2025Review
- Knockout of Sirtuin 3 in endothelial cells impairs endothelial-dependent relaxation and myogenic response in mice.Physiological reports · 2024Article
- Ferrostatin-1 specifically targets mitochondrial iron-sulfur clusters and aconitase to improve cardiac function in Sirtuin 3 cardiomyocyte knockout mice.Journal of molecular and cellular cardiology · 2024Article
- p53 Acetylation Exerts Critical Roles in Pressure Overload-Induced Coronary Microvascular Dysfunction and Heart Failure in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- SIRT3 Deficiency Enhances Ferroptosis and Promotes Cardiac Fibrosis via p53 Acetylation.Cells · 2023Article
- SIRT3/GLUT4 signaling activation by metformin protect against cisplatin-induced ototoxicity in vitro.Archives of toxicology · 2023Article
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- Knockout of TIGAR enhances myocardial phosphofructokinase activity and preserves diastolic function in heart failure.Journal of cellular physiology · 2022Article
- Aging and short-term calorie restriction differently affect the cardiac and skeletal muscle expression of genes regulating energy substrate utilization in male rats.Biogerontology · 2022Article
- The glycolytic process in endothelial cells and its implications.Acta pharmacologica Sinica · 2022Review
- Endothelial Dysfunction in Heart Failure With Preserved Ejection Fraction: What are the Experimental Proofs?Frontiers in physiology · 2022Review
- Emerging Roles of SIRT3 in Cardiac Metabolism.Frontiers in cardiovascular medicine · 2022Review
- The roles and mechanisms of epigenetic regulation in pathological myocardial remodeling.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Background Alterations of energetic metabolism are suggested to be an important contributor to pressure overload (PO)-induced heart failure. Our previous study reveals that knockout of endothelial Sirtuin 3 (SIRT3) alters glycolysis and impairs diastolic function. We hypothesize that endothelial SIRT3 regulates glucose utilization of cardiomyocytes and sensitizes PO-induced heart failure. Methods and Results SIRT3 endothelial cell knockout mice and their control SIRT3 LoxP mice were subjected to PO by transverse aortic constriction for 7 weeks. The ratio of heart weight to tibia length was increased in both strains of mice, in which SIRT3 endothelial cell knockout mice+transverse aortic constriction exhibited more severe cardiac hypertrophy. Coronary blood flow and systolic function were significantly decreased in SIRT3 endothelial cell knockout mice+transverse aortic constriction compared with SIRT3 LoxP mice+transverse aortic constriction, as evidenced by lower systolic/diastolic ratio, ejection fraction, and fractional shortening. PO-induced upregulation of apelin and glucose transporter 4 were significantly reduced in the hearts of SIRT3 endothelial cell knockout mice. In vitro
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.