ArticleLife sciences2021
Development of heart failure with preserved ejection fraction in type 2 diabetic mice is ameliorated by preserving vascular function.
Article in Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- 12(S)-HETE regulates the expression of IL-6 and IL-10 in cardiomyocytes through two distinct receptors, TXA2R and BLT2.Biochemistry and biophysics reports · 2026Article
- Roles of cMyBP-C phosphorylation on cardiac contractile dysfunction inJournal of molecular and cellular cardiology plus · 2024Article
- Transient receptor potential vanilloid type 1: cardioprotective effects in diabetic models.Channels (Austin, Tex.) · 2023Review
- The association between eicosanoids and incident atrial fibrillation in the Framingham Heart Study.Scientific reports · 2022Article
- The Role of Systemic Microvascular Dysfunction in Heart Failure with Preserved Ejection Fraction.Biomolecules · 2022Review
- Endothelial Dysfunction in Heart Failure With Preserved Ejection Fraction: What are the Experimental Proofs?Frontiers in physiology · 2022Review
- TRP Channels as Sensors of Aldehyde and Oxidative Stress.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsHeart failure with preserved ejection fraction (HFpEF) is associated with endothelial dysfunction and is frequent in people with type 2 diabetes mellitus. In diabetic patients, increased levels of the eicosanoid 12-hydroxyeicosatetraenoic acid (12-HETE) are linked to vascular dysfunction. Here, we aimed to identify the importance of 12-HETE in type 2 diabetic patients exhibiting diastolic dysfunction, and mice exhibiting HFpEF and whether targeting 12-HETE is a means to ameliorate HFpEF progression by improving vascular function in diabetes. MATERIAL AND
methodsSubjects with diagnosed type 2 diabetes mellitus and reported diastolic dysfunction or healthy controls were recruited and 12(S)-HETE levels determined by ELISA. 12(S)-HETE levels were determined in type 2 diabetic, leptin receptor deficient mice (LepR KEY
findingsEndothelium-dependent vasodilation and mitochondrial functional capacity both improved in response to either application of ML351 or the V1-cal peptide. Correlating to improved vascular function, mice treated with either pharmacological agent exhibited improved diastolic filling and left ventricular relaxation that correlated with increased myocardial capillary density. SIGNIFICANCE: Our results suggest that 12-HETE may serve as a biomarker indicating endothelial dysfunction and the resulting cardiovascular consequences such as HFpEF in type 2 diabetic patients. Antagonizing 12-HETE is a potent means to causally control HFpEF development and progression in type 2 diabetes by preserving vascular function.
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Registered trials
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