ArticleAmerican journal of physiology. Heart and circulatory physiology2025
Reduced cofilin activity as a mechanism contributing to endothelial cell stiffening in type 2 diabetes.
Article in American journal of physiology. Heart and circulatory physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Beneficial vascular effects of oral phosphatidylserine supplementation in type 2 diabetes.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Trial
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Late-Onset Menopause Attenuates Aortic Stiffness in the Postmenopausal Period.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Cytochalasins Suppress 3D Migration of ECM-Embedded Tumoroids at Non-Toxic Concentrations.International journal of molecular sciences · 2025Article
- LIM kinases in cardiovascular health and disease.Frontiers in physiology · 2024Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
An emerging instigator of endothelial dysfunction in type 2 diabetes (T2D) is the stiffening of the cell. Previous reports suggest that polymerization of filamentous actin (F-actin) is a potential mediator of endothelial stiffening. Actin polymerization is limited by active cofilin, an F-actin-severing protein that can be oxidized, leading to its inactivation and loss of severing capability. Yet, whether these mechanisms are implicated in endothelial stiffening in T2D remains unknown. Herein, we report that endothelial cells exposed to plasma from male and female subjects with T2D, and the aortic endothelium of diabetic male mice (
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.