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ORIGINAL RESEARCH article

Front. Endocrinol.

Sec. Cardiovascular Endocrinology

Volume 16 - 2025 | doi: 10.3389/fendo.2025.1504614

Uric Acid-Induced Cardiomyocytic Polyamines' Insufficience: a Potential Mechanism mediates Cardiomyocytic Injury

Provisionally accepted
Cuiting Lin Cuiting Lin 1Qiang Zheng Qiang Zheng 1Haiyan YU Haiyan YU 1Ting Wu Ting Wu 2Lin Chen Lin Chen 1Weihao Lin Weihao Lin 1Jianxin Pang Jianxin Pang 2*Yang Yang Yang Yang 1*
  • 1 Pingshan Hospital, Southern Medical University, Shenzhen, China, China
  • 2 Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmacy, Southern Medical University, Guangzhou, China

The final, formatted version of the article will be published soon.

    Maintaining polyamines homeostasis is essential for cardiovascular health, whereas elevated uric acid levels are recognized as a significant risk factor for the onset and progression of cardiovascular diseases. However, the interaction between uric acid and the regulation of polyamine homeostasis has not been extensively investigated. The objective of this study was to investigate the influence of uric acid on cardiac polyamines regulation and elucidate the role of polyamines in uric acid induced cardiomyocytic injury. Our study demonstrates that uric acid treatment can alter ornithine metabolism in cardiomyocytes, shifting it from the traditional ornithine cycle towards the polyamine cycle. Upon further investigation, we observed a downregulation of spermidine and spermine levels in the heart tissues of mice with hyperuricemia compared to controls, a phenomenon also recapitulated in cardiomyocytes under uric acid treatment. Notably, exogenous supplementation with spermidine or spermine effectively mitigated the uric acid-induced decline in cardiomyocyte viability and mitochondrial membrane potential. These findings indicate that the uric acid leads to cardiomyocytic polyamines decreasing, thereby insufficient polyamine levels could represent a key mechanism underlying uric acid-induced cardiomyocyte injury. This study not only elucidates the mechanism of uric acid-induced cardiomyocyte injury from a novel perspective but also provides new pharmacological insights and potential intervention strategies for treatment.

    Keywords: Polyamines, Uric Acid, cardiomyocytes, Spermidine, Spermine

    Received: 01 Oct 2024; Accepted: 04 Mar 2025.

    Copyright: © 2025 Lin, Zheng, YU, Wu, Chen, Lin, Pang and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Jianxin Pang, Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmacy, Southern Medical University, Guangzhou, 510000, China
    Yang Yang, Pingshan Hospital, Southern Medical University, Shenzhen, China, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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