ArticleCurrent issues in molecular biology2025
Uric Acid: A New Perspective for Exploring the Pathological Process of Anthracycline-Induced Cardiotoxicity.
Article in Current issues in molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Intravenous Mitochondrial Injection Attenuates Methanol-Induced Cardiotoxicity Through Restoration of Mitochondrial Function and Suppression of Oxidative Stress.Cardiovascular toxicology · 2026Article
- Evaluation of toll-like receptor inhibition by novel thymoquinone analogues as potential remedy for diabetic nephropathy.Molecular diversity · 2026Article
- Gegen Flavonoids and Huangqi Saponins Combination Ameliorates Diabetic Nephropathy By Modulating the Gut-Kidney Axis and Regulating Macrophage Polarization.Applied biochemistry and biotechnology · 2026Article
- Exercise-induced neuropeptidergic and neurochemical neuroadaptation in stress regulation and emotional disorders.Acta neurologica Belgica · 2026Review
- Pollutant-regulated mitophagy: new perspectives in environmental toxicology.Apoptosis : an international journal on programmed cell death · 2026Review
- Amelioration of cisplatin-induced myocardial injury by nanocurcumin through antioxidant, anti-inflammatory, and calcium regulatory mechanisms.Journal of molecular histology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Anthracycline's clinical application is often hampered by severe life-threatening cardiotoxicity, which could result in death in approximately one-third of patients. Previous studies have found that during the anthracycline-induced cardiotoxicity (AIC), uric acid (UA) levels increase abnormally. However, the role of UA in AIC remains elusive. Here, we conducted a correlation analysis between UA and cardiac damage markers (NT-pro-BNP, hs-cTnT, LDH, CRP and hs-CRP) by using the National Health and Nutrition Examination Survey database (NHANES); the results revealed that the elevated UA levels showed significant positive associations with the levels of several cardiac damage markers. Secondly, molecular docking experiments suggested potential binding interactions between UA and BNP, cTnT, CRP, and LDH. Finally, animal experiments were performed to validate this correlation we explored and further validated the effect of UA on AIC by adding or lowering UA in animal models. We observed that under high uric acid (HUA) conditions, AIC not only manifested earlier but also progressed more severely. In contrast, AIC was alleviated under UA clearance conditions. Collectively, these results suggested that HUA might be an important contributing factor in the development and progression of AIC, supporting the further investigation of UA-lowering strategies for potential prevention. This work might offer new prevention and treatment strategies for AIC.
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