ArticleCardiovascular diabetology2025
Diabetes mellitus aggravates myocardial inflammation and oxidative stress in aortic stenosis: a mechanistic link to HFpEF features.
Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026Review
- Mechanobiology of the diabetic cardiomyocyte: insulin signaling, titin elasticity, and multiscale mechanical dysfunction.Biophysical reviews · 2026Review
- Review
- Shared pathophysiological mechanisms between diabetes and calcific aortic valve disease: an immunometabolic perspective.Cardiovascular diabetology · 2026Review
- Association between cardiometabolic index and major adverse cardio-cerebral events and all-cause mortality in patients with degenerative aortic stenosis: a retrospective cohort study.Journal of thoracic disease · 2026Article
- Post-PCI Inflammation and Diastolic Dysfunction in Patients with Metabolic Risk Factors: A Retrospective Observational Study.Medicina (Kaunas, Lithuania) · 2025Observational
- Article
- Apolipoprotein CII: Cornerstone of Pathophysiological Interplay in Aortic Stenosis and type 2 Diabetes Mellitus.Aging and disease · 2025Article
- Mechanism-guided pharmacotherapy for cardiometabolic multimorbidity: from pathophysiology to phenotype-prioritized treatment.Frontiers in endocrinology · 2025Review
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Authors and funding
22 authors.
Funding
Abstract
backgroundPatients diagnosed with both aortic stenosis (AS) and diabetes mellitus (DM) encounter a distinctive set of challenges due to the interplay between these two conditions. This study aimed to investigate the effects of DM on the left ventricle in AS patients, specifically focusing on the inflammatory response, oxidative stress, and their implications for cardiomyocyte function, titin phosphorylation, and the nitric oxide (NO)-soluble guanylyl cyclase (sGC)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signaling pathway. METHODS AND
resultsLeft ventricular myocardial biopsies (in total: n = 28) were obtained from patients with diabetic AS (n = 11) and compared with those from non-diabetic AS patients (n = 17). Enzyme-linked immunosorbent assay (ELISA) demonstrated significantly elevated levels of pro-inflammatory mediators, including high mobility group box protein 1 (HMGB1) and calprotectin, as well as receptors associated with the inflammatory response, such as Toll-like receptor 2 (TLR2), 4 (TLR4), and receptor for advanced glycation endproducts (RAGE). These were correlated with an enhanced NOD-like receptor protein 3 (NLRP3) inflammasome and the release of interleukins (IL) 1, 6, and 18 in diabetic AS patients compared to their non-diabetic counterparts. Additionally, in the diabetic AS cohort, there was an increase in oxidative stress markers (hydrogen peroxide (H
conclusionDM exacerbates inflammation and oxidative stress in AS patients, leading to impaired NO-sGC-cGMP-PKG signaling and increased cardiomyocyte F
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