ReviewCell death & disease2023
Vascular nitric oxide resistance in type 2 diabetes.
Review in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
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- Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.Electrolyte & blood pressure : E & BP · 2026Review
- The Effects of GLP-1 Receptor Agonists on Retinal Microvascular Alterations.Biomedicines · 2026Review
- Higher salivary nitrite is associated with improved glycemic control and insulin sensitivity in patients with type 2 diabetes.Nutrition & metabolism · 2026Article
- Impact of Cardiometabolic Risk Markers on the Incidence and Progression Arterial Stiffness in Patients With Prediabetes.Journal of diabetes · 2026Article
- Review
- Functional Segregation of Pancreatic Microcirculation Reveals Sex-Dependent Microhemodynamic Signatures.Comprehensive Physiology · 2026Article
- Translocator Protein Modulation by PK11195 and NO Synthase Inhibition Affect Cardiac Oxidative Stress and Cardiometabolic and Inflammatory Markers in Isoprenaline-Induced Rat Myocardial Injury.International journal of molecular sciences · 2026Article
- In-Stent Restenosis Pathophysiology and Risk Factors: A Comprehensive Review.Medicina (Kaunas, Lithuania) · 2026Review
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Association of the triglyceride glucose index and its related indices with coronary artery disease risk: mediation by glycated haemoglobin.Frontiers in endocrinology · 2026Article
- Cardiovascular Dysfunction in Type 2 Diabetes: The Role of MicroRNAs.Handbook of experimental pharmacology · 2026Review
- Maternal Gestational Diabetes Impairs Fetoplacental Insulin-Induced Vasodilation via AKT/eNOS Pathway and Reduces Placental Efficiency.International journal of molecular sciences · 2025Article
- The association between insulin resistance assessed by estimated glucose disposal rate and stroke prevalence and mortality in non-diabetic people: evidence from two prospective cohorts.Diabetology & metabolic syndrome · 2025Article
- Association of triglyceride-glucose index with risk of cardiovascular disease among patients with prediabetes: population based prospective cohort study.BMC cardiovascular disorders · 2025Article
- The Impact of Glucagon-like Peptide-1 Receptor Agonists on Erectile Function: Friend or Foe?Biomolecules · 2025Review
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Sex- and Dose-Dependent Effect of L-Citrulline on Body Weight and Food Intake in Obese Type 2 Diabetic Rats.International journal of endocrinology and metabolism · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular nitric oxide (NO•) resistance, manifested by an impaired vasodilator function of NO• in both the macro- and microvessels, is a common state in type 2 diabetes (T2D) associated with developing cardiovascular events and death. Here, we summarize experimental and human evidence of vascular NO• resistance in T2D and discuss its underlying mechanisms. Human studies indicate a ~ 13-94% decrease in the endothelium (ET)-dependent vascular smooth muscle (VSM) relaxation and a 6-42% reduced response to NO• donors, i.e., sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), in patients with T2D. A decreased vascular NO• production, NO• inactivation, and impaired responsiveness of VSM to NO• [occurred due to quenching NO• activity, desensitization of its receptor soluble guanylate cyclase (sGC), and/or impairment of its downstream pathway, cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG)] are the known mechanisms underlying the vascular NO• resistance in T2D. Hyperglycemia-induced overproduction of reactive oxygen species (ROS) and vascular insulin resistance are key players in this state. Therefore, upregulating vascular NO• availability, re-sensitizing or bypassing the non-responsive pathways to NO•, and targeting key vascular sources of ROS production may be clinically relevant pharmacological approaches to circumvent T2D-induced vascular NO• resistance.
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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.