ArticleiScience2023
URAT1 is expressed in cardiomyocytes and dotinurad attenuates the development of diet-induced metabolic heart disease.
Article in iScience, 2023. 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, 11 citations in OpenAlex.
- Redefining Uric Acid and Cardiovascular Risk: Vascular Gout and Crystal-Driven Vascular Inflammation in Asymptomatic Hyperuricemia.JACC. Asia · 2026Review
- The effects of GLUT9 and URAT1 inhibitors on cardiovascular diseases: a drug-targeted Mendelian randomization study.International urology and nephrology · 2025Article
- Synthetic strategies towards benzothiazole-based compounds of therapeutic potency: experimental, investigational and approved drugs.RSC advances · 2025Review
- Inflammageing, a targetable pathway for preventing cardiovascular diseases.Cardiovascular research · 2025Review
- Extra-renal role of urate transporter-1 in diabetes.World journal of diabetes · 2025Review
- Comparative assessment of the effects of dotinurad and febuxostat on the renal function in chronic kidney disease patients with hyperuricemia.Scientific reports · 2025Article
- Research progress on multidimensional intervention strategies for hyperuricemia: Western medicine, Traditional Chinese Medicine, and emerging therapies.Frontiers in endocrinology · 2025Review
- Narrative Review of Immunomodulatory and Anti-inflammatory Effects of Sodium-Glucose Cotransporter 2 Inhibitors: Unveiling Novel Therapeutic Frontiers.Kidney international reports · 2024Review
- Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently reported that the selective inhibition of urate transporter-1 (URAT1), which is primarily expressed in the kidneys, ameliorates insulin resistance by attenuating hepatic steatosis and improving brown adipose tissue function in diet-induced obesity. In this study, we evaluated the effects of dotinurad, a URAT1-selective inhibitor, on the hearts of high-fat diet (HFD)-fed obese mice for 16-20 weeks and on neonatal rat cardiomyocytes (NRCMs) exposed to palmitic acid. Outside the kidneys, URAT1 was also expressed in cardiomyocytes and indeed worked as a uric acid transporter. Dotinurad substantially attenuated HFD-induced cardiac fibrosis, inflammatory responses, and cardiac dysfunction. Intriguingly, among various factors related to the pathophysiology of diet-induced obesity, palmitic acid significantly increased URAT1 expression in NRCMs and subsequently induced apoptosis, oxidative stress, and inflammatory responses via MAPK pathway, all of which were reduced by dotinurad. These results indicate that URAT1 is a potential therapeutic target for metabolic heart disease.
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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 OpenQuestion graph.