SGLT2 Inhibitors as Endothelial Protectors: Mechanisms of Vascular Restoration in Type 2 Diabetes
- 1Grupo de Investigación en Enfermedades Cardiorrenales y Metabólicas, Departamento de Medicina y Cirugía, Facultad de Ciencias de la Salud, Universidad Cardenal Herrera-CEU, CEU Universities, C/Santiago Ramón y Cajal S/N, 46115 Valencia, Spain
Abstract
Endothelial dysfunction is a fundamental catalyst of atherosclerosis and cardiovascular mortality in type 2 diabetes mellitus (T2DM). While sodium-glucose co-transporter 2 inhibitors (SGLT2is) provide robust cardioprotection, whether these benefits stem from direct vasculature effects or from secondary systemic hemodynamics remains an active translational frontier. At the cellular level, preclinical data suggests that SGLT2is may modulate homeostatic pathways by suppressing NADPH oxidase-mediated oxidative stress, attenuating NF-κB/NLRP3-driven inflammatory cascades, and preserving endothelial nitric oxide synthase (eNOS) activity. In clinical cohorts, these molecular actions correlate with heterogeneous changes in flow-mediated dilation (FMD) and reductions in arterial stiffness. However, translating these cellular findings to macrovascular outcomes is highly confounded by concurrent volume contraction, blood pressure lowering and metabolic shifts.
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BibTeX
@article{okojie2026sglt2,
title = {{SGLT2 Inhibitors as Endothelial Protectors: Mechanisms of Vascular Restoration in Type 2 Diabetes}},
author = {Owahabanun-Joshua Okojie and Ana Checa-Ros and Luis D’Marco},
journal = {Metabolites},
year = {2026},
month = oct,
doi = {10.3390/metabo16110824},
url = {https://www.mdpi.com/2218-1989/16/11/824},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - SGLT2 Inhibitors as Endothelial Protectors: Mechanisms of Vascular Restoration in Type 2 Diabetes
AU - Owahabanun-Joshua Okojie
AU - Ana Checa-Ros
AU - Luis D’Marco
PY - 2026
DA - 2026/10/28
JO - Metabolites
DO - 10.3390/metabo16110824
UR - https://www.mdpi.com/2218-1989/16/11/824
AB - Endothelial dysfunction is a fundamental catalyst of atherosclerosis and cardiovascular mortality in type 2 diabetes mellitus (T2DM). While sodium-glucose co-transporter 2 inhibitors (SGLT2is) provide robust cardioprotection, whether these benefits stem from direct vasculature effects or from secondary systemic hemodynamics remains an active translational frontier. At the cellular level, preclinical data suggests that SGLT2is may modulate homeostatic pathways by suppressing NADPH oxidase-mediated oxidative stress, attenuating NF-κB/NLRP3-driven inflammatory cascades, and preserving endothelial nitric oxide synthase (eNOS) activity. In clinical cohorts, these molecular actions correlate with heterogeneous changes in flow-mediated dilation (FMD) and reductions in arterial stiffness. However, translating these cellular findings to macrovascular outcomes is highly confounded by concurrent volume contraction, blood pressure lowering and metabolic shifts.
SN - 2218-1989
ER -