ArticleFrontiers in pharmacology2020
Erythrocytes Induce Endothelial Injury in Type 2 Diabetes Through Alteration of Vascular Purinergic Signaling.
Article in Frontiers in pharmacology, 2020. 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.
- Insulin facilitates entry of calcium ions into human and murine erythrocytes via Piezo1: a newly identified mechanism with implications for type 2 diabetes.The FEBS journal · 2025Article
- Impact of Estrogen on Purinergic Signaling in Microvascular Disease.International journal of molecular sciences · 2025Review
- New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications.International journal of molecular sciences · 2024Review
- Unexplored Roles of Erythrocytes in Atherothrombotic Stroke.Neurology international · 2023Review
- Recent advances in molecular biology of metabolic syndrome pathophysiology: endothelial dysfunction as a potential therapeutic target.Journal of diabetes and metabolic disorders · 2022Review
- Purinergic activation in response to hemodynamic force directs heart valve development.Purinergic signalling · 2022Article
- Purinergic interplay between erythrocytes and platelets in diabetes-associated vascular dysfunction.Purinergic signalling · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
It is well established that altered purinergic signaling contributes to vascular dysfunction in type 2 diabetes (T2D). Red blood cells (RBCs) serve as an important pool for circulating ATP and the release of ATP from RBCs in response to physiological stimuli is impaired in T2D. We recently demonstrated that RBCs from patients with T2D (T2D RBC) serve as key mediators of endothelial dysfunction. However, it remains unknown whether altered vascular purinergic signaling is involved in the endothelial dysfunction induced by dysfunctional RBCs in T2D. Here, we evaluated acetylcholine-induced endothelium-dependent relaxation (EDR) of isolated rat aortas after 18 h
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