ArticleCurrent pharmaceutical design2025
Retinoic Acid Improves Vascular Endothelial Dysfunction by Inhibiting PI3K/AKT/YAP-mediated Ferroptosis in Diabetes Mellitus.
Article in Current pharmaceutical design, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Liposome-iRGD loaded with astragaloside IV alleviates the functional damage of endothelial progenitor cells via the Hippo-YAP/TAZ signaling pathway.In vitro cellular & developmental biology. Animal · 2026Article
- The therapeutic potential of vitamins as nutrients in food for anti-inflammatory and anti-oxidative stress in liver fibrosis diseases.Frontiers in nutrition · 2026Review
- Ferroptosis in the pathogenesis of diabetic cardiomyopathy: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Effects of realgar-indigo naturalis formula on a zebrafish tumor xenograft model induced by human acute promyelocytic leukemia cells: antitumor activity, hepatotoxicity, and transcriptomic analysis.Frontiers in pharmacology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundVascular endothelial dysfunction is the initial factor involved in cardiovascular injury in patients with diabetes. Retinoic acid is involved in improving vascular complications with diabetes, but its protective mechanism is still unclear. This study aimed to evaluate the effect and mechanism of All-trans Retinoic Acid (ATRA) on endothelial dysfunction induced by diabetes.
methodsIn the present study, streptozotocin (STZ)-induced diabetic rats and high glucose (HG)-induced human umbilical vein endothelial cells (HUVECs) were observed, and the effects of ATRA on HG-induced endothelial dysfunction and ferroptosis were evaluated.
resultsATRA treatment improved impaired vasorelaxation in diabetic aortas in an endothelium-dependent manner, and this effect was accompanied by an increase in the NO concentration and eNOS expression. Ferroptosis, characterized by lipid peroxidation and iron overload induced by HG, was improved by ATRA administration, and a ferroptosis inhibitor (ferrostatin-1, Fer-1) improved endothelial function to a similar extent as ATRA. In addition, the inactivation of phosphoinositol-3-kinase (PI3K)/protein kinases B (AKT) and Yes-associated Protein (YAP) nuclear localization induced by HG were reversed by ATRA administration. Vascular ring relaxation experiments showed that PI3K/AKT activation and YAP inhibition had similar effects on ferroptosis and endothelial function. However, the vasodilative effect of retinoic acid was affected by PI3K/AKT inhibition, and the inhibitory effects of ATRA on ferroptosis and the improvement of endothelial function were dependent on the retinoic acid receptor.
conclusionATRA could improve vascular endothelial dysfunction by inhibiting PI3K/AKT/YAP-mediated ferroptosis induced by HG, which provides a new idea for the treatment of vascular lesions in diabetes.
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