Article

Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1

2023-04-21

Abstract excerpt

<h4>Rationale</h4> Obesity increases the risk of cardiovascular disease (CVD) through mechanisms that remain incompletely defined. Metabolic dysfunction, especially hyperglycemia, is thought to be a major contributor but how glucose impacts vascular function is unclear. Galectin-3 (GAL3) is a sugar binding lectin upregulated by hyperglycemia but its role as a causative mechanism of CVD remains poorly understood....

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: d929da3f-d38a-5582-91fb-f1e41daae164
DOI: 10.1101/2023.04.19.537592

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Galectin-3 Mediates Vascular Dysfunction in Obesity by Regulating NADPH Oxidase 1DOI 10.1101/2023.04.19.537592Read

Perturbing O-GlcNAcase Modulates the Expression and Distribution of Galectin-3Semantic proximity Read

Transcriptional analysis of the endothelial response to diabetes reveals a role for galectin-3Semantic proximity Read

Genetic Deletion of NADPH Oxidase 1 Rescues Microvascular Function in Mice With Metabolic DiseaseSemantic proximity Read

Nox2-derived superoxide contributes to cerebral vascular dysfunction in diet-induced obesity.Semantic proximity Read

Galectin-3 Impairs Calcium Transients and β-Cell FunctionSemantic proximity Read

Functional relevance of genetic variations of endothelial nitric oxide synthase and vascular endothelial growth factor in diabetic coronary microvessel dysfunction.Semantic proximity Read

Suppression of Endothelial AGO1 Promotes Adipose Tissue Browning and Improves Metabolic Dysfunction.Semantic proximity Read

Evaluation of systemic endothelial-dependent and endothelial-independent microvascular reactivity in metabolically healthy obesity: An observational study.Semantic proximity Read

Blocking endothelial TRPV4-Nox2 interaction helps reduce ROS production and inflammation, and improves vascular function in obese mice.Semantic proximity Read

Toll-Like Receptor 2 (TLR2) Knockout Abrogates Diabetic and Obese Phenotypes While Restoring Endothelial Function via Inhibition of NOX1.Semantic proximity Read

Repeated Glucose Spikes and Insulin Resistance Synergistically Increase Endothelial Function Vulnerability to High Glucose Levels through Redox Imbalance, and Bardoxolone Methyl (CDDO-Me) Ameliorates Endothelial DysfunctionSemantic proximity Read

Diabetic eNOS knockout mice develop distinct macro- and microvascular complications.Semantic proximity Read