Endothelial Metabolism in Health and Disease

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 3118

Special Issue Editors


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Guest Editor
Department of Pharmacology, Normandie University, UNIROUEN, INSERM U1096, CHU Rouen, F-76000 Rouen, France
Interests: Cardiovascular system; endothelium; bioinformatics; pharmaco-metrics; pharmacology.

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Guest Editor
Center for Systems Biology, University of Iceland, 101 Reykjavík, Iceland
Interests: Cardiovascular system; endothelium; bioinformatics; pharmaco-metrics; pharmacology

Special Issue Information

Dear Colleagues,

Metabolism is paramount to endothelium and vascular function. Indeed, metabolome profiling has recently become an essential aspect to many studies aiming to deliver quantitative and mechanistic understanding of health and disease conditions. Metabolomics is a consolidated powerful tool to decipher complex mechanisms that result in endothelial dysfunction. Furthermore, computational approaches such as genome-scale metabolic modeling represent additional key tools to understand endothelial metabolic and phenotypic transitions. Since the endothelium constitutes an active interface between circulating blood, lymph and all organs, metabolome profile quantification has the potential to generate new insights into a plethora of pathological conditions including sepsis, diabetes, cardiovascular diseases, cancer and infectious diseases such as COVID-19. Insights obtained from the application of metabolomics techniques to better understand endothelial function pave the way to reveal novel therapeutic targets, in addition to detecting early metabolic signs of disease transition.

The scope of this Special Issue “Endothelial Metabolism in Health and Disease” is devoted to topics that include metabolic studies of human and murine endothelium, endothelial cell cultures, the cardiovascular system, computational genome-scale metabolic analyses, lipidomics, metabolomics, as well as innovative bioanalysis and data integration for the discovery of therapeutic targets that may prevent or decrease endothelial dysfunction.

Dr. Thomas Duflot
Dr. Adrian Lopez Garcia De Lomana
Guest Editors

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Keywords

  • metabolomics
  • mass spectrometry
  • genome-scale metabolic modeling
  • endothelial function
  • biomarkers
  • vascular function
  • novel therapeutic targets
  • cardiovascular diseases

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Published Papers (1 paper)

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Review

22 pages, 2111 KiB  
Review
Significance of Endothelial Dysfunction Amelioration for Sodium–Glucose Cotransporter 2 Inhibitor-Induced Improvements in Heart Failure and Chronic Kidney Disease in Diabetic Patients
by Hidekatsu Yanai, Hiroki Adachi, Mariko Hakoshima and Hisayuki Katsuyama
Metabolites 2023, 13(6), 736; https://doi.org/10.3390/metabo13060736 - 8 Jun 2023
Cited by 5 | Viewed by 2157
Abstract
Beyond lowering plasma glucose levels, sodium–glucose cotransporter 2 inhibitors (SGLT2is) significantly reduce hospitalization for heart failure (HF) and retard the progression of chronic kidney disease (CKD) in patients with type 2 diabetes. Endothelial dysfunction is not only involved in the development and progression [...] Read more.
Beyond lowering plasma glucose levels, sodium–glucose cotransporter 2 inhibitors (SGLT2is) significantly reduce hospitalization for heart failure (HF) and retard the progression of chronic kidney disease (CKD) in patients with type 2 diabetes. Endothelial dysfunction is not only involved in the development and progression of cardiovascular disease (CVD), but is also associated with the progression of CKD. In patients with type 2 diabetes, hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia induce the development of endothelial dysfunction. SGLT2is have been shown to improve endothelial dysfunction, as assessed by flow-mediated vasodilation, in individuals at high risk of CVD. Along with an improvement in endothelial dysfunction, SGLT2is have been shown to improve oxidative stress, inflammation, mitochondrial dysfunction, glucotoxicity, such as the advanced signaling of glycation end products, and nitric oxide bioavailability. The improvements in endothelial dysfunction and such endothelium-derived factors may play an important role in preventing the development of coronary artery disease, coronary microvascular dysfunction and diabetic cardiomyopathy, which cause HF, and play a role in retarding CKD. The suppression of the development of HF and the progression of CKD achieved by SGLT2is might have been largely induced by their capacity to improve vascular endothelial function. Full article
(This article belongs to the Special Issue Endothelial Metabolism in Health and Disease)
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