ArticleCells2019
NLRP3 Inflammasome and Mineralocorticoid Receptors Are Associated with Vascular Dysfunction in Type 2 Diabetes Mellitus.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 68 citations in OpenAlex.
- Proteomic Analysis of Effects of Spironolactone in Heart Failure With Preserved Ejection Fraction.Circulation. Heart failure · 2022Trial
- Aldosterone-mineralocorticoid receptor signaling and residual cardiorenal risk in type 2 diabetes.Acta diabetologica · 2026Review
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Review
- Interplay Between the Mineralocorticoid System, Inflammation, Hypertension, and Kidney Disease.Kidney360 · 2025Review
- Current Landscape of the Interrelationship Between Periodontitis, Type 2 Diabetes Mellitus, and COVID-19.International journal of molecular sciences · 2025Review
- PCSK9 Inhibitors: A Potential Priority Choice for Lipid Management in Patients with Diabetic Kidney Disease.Drugs · 2025Review
- Exploring Anti-Inflammatory Treatment as Upstream Therapy in the Management of Atrial Fibrillation.Journal of clinical medicine · 2025Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- Effect ofInternational journal of food science · 2025Article
- Esaxerenone Inhibits Interferon-γ Induced Pyroptosis of Macrophages in the Lungs of Aldosterone-treated Mice.Inflammation · 2024Article
- Aldosterone, Methylglyoxal, and Glycated Albumin Interaction with Macrophage Cells Affects Their Viability, Activation, and Differentiation.ACS omega · 2024Article
- Crosstalk between Aldosterone and Glycation through Rac-1 Induces Diabetic Nephropathy.ACS omega · 2023Article
- Suppressed vascular Rho-kinase activation is a protective cardiovascular mechanism in obese female mice.Bioscience reports · 2023Article
- New retinal findings in NLRP3-associated autoinflammatory disease.Orphanet journal of rare diseases · 2023Article
- Tricyclic antidepressants induce liver inflammation by targeting NLRP3 inflammasome activation.Cell communication and signaling : CCS · 2023Article
- Inhibitors of the NLRP3 inflammasome pathway as promising therapeutic candidates for inflammatory diseases (Review).International journal of molecular medicine · 2023Review
- The Synthetic Flavonoid Hidrosmin Improves Endothelial Dysfunction and Atherosclerotic Lesions in Diabetic Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Dexamethasone and potassium canrenoate alleviate hyperalgesia by competitively regulating IL-6/JAK2/STAT3 signaling pathway during inflammatory pain in vivo and in vitro.Immunity, inflammation and disease · 2022Article
- Diabetes Mellitus Promotes the Development of Atherosclerosis: The Role of NLRP3.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone excess aggravates endothelial dysfunction in diabetes and hypertension by promoting the increased generation of reactive oxygen species, inflammation, and insulin resistance. Aldosterone activates the molecular platform inflammasome in immune system cells and contributes to vascular dysfunction induced by the mineralocorticoid hormone. It is unclear as to whether the NLRP3 inflammasome associated with the mineralocorticoid receptor contributes to vascular dysfunction in diabetic conditions. Here, we tested the hypothesis that an excess of aldosterone induces vascular dysfunction in type 2 diabetes, via the activation of mineralocorticoid receptors (MR) and assembly of the NLRP3 inflammasome. Mesenteric resistance arteries from control (db/m) and diabetic (db/db) mice treated with vehicle, spironolactone (MR antagonist) or an NLRP3 selective inhibitor (MCC950) were used to determine whether NLRP3 contributes to diabetes-associated vascular dysfunction. Db/db mice exhibited increased vascular expression/activation of caspase-1 and IL-1β, increased plasma IL-1β levels, active caspase-1 in peritoneal macrophages, and reduced acetylcholine (ACh) vasodilation, compared to db/m mice. Treatment of db/db mice with spironolactone and MCC950 decreased plasma IL-1β and partly restored ACh vasodilation. Spironolactone also reduced active caspase-1-positive macrophages in db/db mice, events that contribute to diabetes-associated vascular changes. These data clearly indicate that MR and NLRP3 activation contribute to diabetes-associated vascular dysfunction and pro-inflammatory phenotype.
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