What does this research mean for the field?

High uric acid levels are associated with earlier onset and more severe progression of anthracycline-induced cardiotoxicity in animal models. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.CHALLENGES_CONSENSUS.

What question did this study set out to answer?

To explore the relationship between uric acid levels and anthracycline-induced cardiotoxicity.

January 10, 2026Current Issues in Molecular Biology0 citationsOpen Access

Uric Acid: A New Perspective for Exploring the Pathological Process of Anthracycline-Induced Cardiotoxicity

YRYifei RaoJiangxi University of Traditional Chinese Medicine YWYu WangTianjin University of Science and Technology YLYadi LiuBeijing University of Chinese Medicine

Key Result

High uric acid levels were associated with earlier onset and more severe progression of anthracycline-induced cardiotoxicity in animal models.

Key Points

To explore the relationship between uric acid levels and anthracycline-induced cardiotoxicity.
Conducted correlation analyses using the NHANES database
Performed molecular docking experiments to assess interactions
Conducted animal experiments to validate findings regarding uric acid's effects
Elevated uric acid levels show significant positive associations with cardiac damage markers
Molecular docking suggests binding interactions between uric acid and several heart-related proteins
High uric acid conditions exacerbate cardiotoxicity, while UA clearance alleviates it

Structured PICO

Does elevated uric acid exacerbate the severity and progression of anthracycline-induced cardiotoxicity?

Population

NHANES database participants and animal models of anthracycline-induced cardiotoxicity

Intervention

Addition of uric acid (high uric acid conditions)

Comparator

Uric acid clearance conditions (lowering uric acid)

Outcome

Levels of cardiac damage markers (NT-pro-BNP, hs-cTnT, LDH, CRP, hs-CRP) and severity/progression of anthracycline-induced cardiotoxicitysurrogate

Elevated uric acid exacerbates anthracycline-induced cardiotoxicity, suggesting that uric acid-lowering therapies could serve as a novel preventive strategy.

Main Result

Absolute Event Rate: 0% vs 0%

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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