ArticleCardiovascular drugs and therapy2024
Insulin Resistance Triggers Atherosclerosis: Caveolin 1 Cooperates with PKCzeta to Block Insulin Signaling in Vascular Endothelial Cells.
Article in Cardiovascular drugs and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Mortality and cardiovascular risk of triglyceride-glucose and derived indices in cardiovascular-kidney-metabolic syndrome stages 0-3: a dose-response meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Angiotensin (1-7) improves diabetes mellitus-induced erectile dysfunction in rats by modulating the Cav-1/eNOS signaling pathway.Sexual medicine · 2026Article
- Antioxidants as a Link Between Diabetes and Potential Plant-Based Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Plant by-products as a valuble source of natural antiglycemic compounds: Economic aspects and alternative raw material sources.Journal of food and drug analysis · 2026Review
- From Metabolism to Mind: The Cardio-Metabolic-Brain Axis and the Role of Insulin Resistance-A Review.Biomedicines · 2026Review
- Identification and Functional Characterization of COPD Molecular Subtypes Based on Oxeiptosis-Related Genes via WGCNA and Machine Learning.International journal of chronic obstructive pulmonary disease · 2026Article
- The Thigh Saphenous Vein Versus the Calf Saphenous Vein: Searching for the Optimal Conduit for Coronary Artery Bypass Grafting.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2025Observational
- Safflower injection against obesity-induced mice podocyte injury by improving insulin resistance through increasing renal INSR and eNOS expression.Renal failure · 2025Article
- Changes in the estimated glucose disposal rate and incident cardiovascular disease in patients with cardiovascular-kidney-metabolic syndrome stages 0-3: a prospective cohort study in China.BMC cardiovascular disorders · 2025Article
- Unraveling the metabolic pathways between atherosclerosis and sarcopenia.Frontiers in endocrinology · 2025Review
- Relationship Between a Novel Model of Insulin Sensitivity and Arterial Stiffness in Non-Obese Patients with Type 2 Diabetes: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- TyG-BMI as a predictor of ischemic stroke over 10 years in middle-aged and older adults: findings from the China cardiometabolic disease and cancer cohort (4C) study.Frontiers in neurology · 2025Article
- Triglyceride-glucose index as a novel prognostic biomarker for coronary artery disease: evidence from a large-scale prospective cohort study.Frontiers in endocrinology · 2025Article
- Associations between estimated glucose disposal rate and arterial stiffness and mortality among US adults with non-alcoholic fatty liver disease.Frontiers in endocrinology · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo date, therapies for endothelial dysfunction have primarily focused on ameliorating identified atherosclerosis (AS) risk factors rather than explicitly addressing endothelium-based mechanism. An in-depth exploration of the pathological mechanisms of endothelial injury was performed herein.
methodsAortic caveolin 1 (Cav1) knockdown was achieved in mice using lentivirus, and AS was induced using a high-fat diet. Mouse body weight, blood glucose, insulin, lipid parameters, aortic plaque, endothelial injury, vascular nitric oxide synthase (eNOS), injury marker, and oxidative stress were examined. The effect of Cav1 knockdown on the content of PKCzeta and PI3K/Akt/eNOS pathway-related protein levels, as well as PKCzeta binding to Akt, was studied. ZIP, a PKCzeta inhibitor, was utilized to treat HUVECs in vitro, and the effect of ZIP on cell viability, inflammatory response, oxidative stress, and Akt activation was evaluated.
resultsCav1 knockdown had no significant effect on body weight or blood glucose in mice over an 8-week period, whereas drastically reduced insulin, lipid parameters, endothelial damage, E-selectin, and oxidative stress and elevated eNOS levels. Moreover, Cav1 knockdown triggered decreased PKCzeta enrichment and the activation of the PI3K/Akt/eNOS pathway. PKCzeta has a positive effect on cells without being coupled by Cav1, and ZIP had no marked influence on PKCzeta-Akt binding following Cav1/PKCzeta coupling.
conclusionCav1/PKCzeta coupling antagonizes the activation of PI3K on Akt, leading to eNOS dysfunction, insulin resistance, and endothelial cell damage.
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