ArticleInternational journal of cardiology2018
Inhibition of prolyl hydroxylases alters cell metabolism and reverses pre-existing diastolic dysfunction in mice.
Article in International journal of cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- 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
- TIGAR Deficiency Blunts Angiotensin-II-Induced Cardiac Hypertrophy in Mice.International journal of molecular sciences · 2024Article
- Article
- Knockout of TIGAR enhances myocardial phosphofructokinase activity and preserves diastolic function in heart failure.Journal of cellular physiology · 2022Article
- Regulatory role of TIGAR on endothelial metabolism and angiogenesis.Journal of cellular physiology · 2021Article
- A Sex-Specific Role of Endothelial Sirtuin 3 on Blood Pressure and Diastolic Dysfunction in Female Mice.International journal of molecular sciences · 2020Article
- Article
- Histone Acetyltransferase p300 Inhibitor Improves Coronary Flow Reserve in SIRT3 (Sirtuin 3) Knockout Mice.Journal of the American Heart Association · 2020Article
- Endothelial Sirtuin 3 Dictates Glucose Transport to Cardiomyocyte and Sensitizes Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2020Article
- Danqi Pill Protects Against Heart Failure Post-Acute Myocardial InfarctionFrontiers in pharmacology · 2020Article
- Sirtuin 3, Endothelial Metabolic Reprogramming, and Heart Failure With Preserved Ejection Fraction.Journal of cardiovascular pharmacology · 2019Review
- Microvascular Rarefaction and Heart Failure With Preserved Ejection Fraction.Frontiers in cardiovascular medicine · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDiastolic dysfunction is emerging as a leading cause of heart failure in aging population. Induction of hypoxia tolerance and reprogrammed cell metabolism have emerged as novel therapeutic strategies for the treatment of cardiovascular diseases. METHODS AND
resultsIn the present study, we showed that deletion of sirtuin 3 (SIRT3) resulted in a diastolic dysfunction together with a significant increase in the expression of prolyl hydroxylases (PHD) 1 and 2. We further investigated the involvement of PHD in the development of diastolic dysfunction by treating the 12-14 months old mice with a PHD inhibitor, dimethyloxalylglycine (DMOG) for 2 weeks. DMOG treatment increased the expression of hypoxia-inducible factor (HIF)-1α in the endothelium of coronary arteries. This was accompanied by a significant improvement of coronary flow reserve and diastolic function. Inhibition of PHD altered endothelial metabolism by increasing glycolysis and reducing oxygen consumption. Most importantly, treatment with DMOG completely reversed the pre-existing diastolic dysfunction in the endothelial-specific SIRT3 deficient mice.
conclusionsOur findings demonstrate that inhibition of PHD and reprogrammed cell metabolism can reverse the pre-existed diastolic dysfunction in SIRT3 deficient mice. Our study provides a potential therapeutic strategy of induction of hypoxia tolerance for patients with diastolic dysfunction associated with coronary microvascular dysfunction, especially in the aging population with reduced SIRT3.
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