ArticleJournal of molecular and cellular cardiology2019
Requisite roles of LOX-1, JNK, and arginase in diabetes-induced endothelial vasodilator dysfunction of porcine coronary arterioles.
Article in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Inhibition in Type 2 Diabetes: Phase 1 Results.Journal of the American Heart Association · 2023Trial
- Serotonin Signaling and Vascular Reactivity in Cardiometabolic Disease and Cardiac Surgery.Cells · 2026Review
- AGGF1-primed endothelial progenitor cells alleviate ischaemia-reperfusion injury in diabetic hearts.Scientific reports · 2025Article
- Lipids and Inflammation: Novel Molecular Targets and Therapeutic Implications.Current medicinal chemistry · 2025Review
- Therapeutic Effects of Proanthocyanidins on Diabetic Erectile Dysfunction in Rats.International journal of molecular sciences · 2024Article
- TXNIP in liver sinusoidal endothelial cells ameliorates alcohol-associated liver disease via nitric oxide production.International journal of biological sciences · 2024Article
- HInternational journal of molecular sciences · 2022Article
- The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications.International journal of molecular sciences · 2022Review
- Arginase: Biological and Therapeutic Implications in Diabetes Mellitus and Its Complications.Oxidative medicine and cellular longevity · 2022Review
- Article
- Activation of Coronary Arteriolar PKCβ2 Impairs Endothelial NO-Mediated Vasodilation: Role of JNK/Rho Kinase Signaling and Xanthine Oxidase Activation.International journal of molecular sciences · 2021Article
- Role of LOX-1 (Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1) as a Cardiovascular Risk Predictor: Mechanistic Insight and Potential Clinical Use.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Role of Arginase in Selective Impairment of Endothelium-Dependent Nitric Oxide Synthase-Mediated Dilation of Retinal Arterioles during Early Diabetes.Investigative ophthalmology & visual science · 2020Article
- Qianlie Beixi Capsules Ameliorate Diabetes-Induced Erectile Dysfunction via Modulation of the HIF-1α/VEGF Signaling Pathway: Evidence From an in Vivo Study.American journal of men's healthArticle
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7 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is associated with cardiac inflammation and impaired endothelium-dependent coronary vasodilation, but molecular mechanisms involved in this dysfunction remain unclear. We examined contributions of inflammatory molecules lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), stress-activated kinases (c-Jun N-terminal kinase [JNK] and p38), arginase, and reactive oxygen species to coronary arteriolar dysfunction in a porcine model of type 1 diabetes. Coronary arterioles were isolated from streptozocin-induced diabetic pigs and control pigs for vasoreactivity and molecular/biochemical studies. Endothelium-dependent nitric oxide (NO)-mediated vasodilation to serotonin was diminished after 2 weeks of diabetes, without altering endothelium-independent vasodilation to sodium nitroprusside. Superoxide scavenger TEMPOL, NO precursor L-arginine, arginase inhibitor nor-NOHA, anti-LOX-1 antibody or JNK inhibitors SP600125 and BI-78D3 improved dilation of diabetic vessels to serotonin. However, hydrogen peroxide scavenger catalase, anti-IgG antibody or p38 kinase inhibitor SB203580 had no effect. Combined inhibition of arginase and superoxide levels did not further improve vasodilation. Arginase-I mRNA expression, LOX-1 and JNK protein expression, and superoxide levels were elevated in diabetic arterioles. In conclusion, sequential activation of LOX-1, JNK, and L-arginine consuming enzyme arginase-I in diabetes elicits superoxide-dependent oxidative stress and impairs endothelial NO-mediated dilation in coronary arterioles. Therapeutic targeting of these adverse vascular molecules may improve coronary arteriolar function during diabetes.
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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.