ArticleAnnals of translational medicine2020
Uric acid preconditioning alleviated doxorubicin induced JNK activation and Cx43 phosphorylation associated cardiotoxicity via activation of AMPK-SHP2 signaling pathway.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- DUSP1 alleviates LPS-induced acute lung injury by inhibiting the SHP2-JNK axis and mitochondrial apoptosis.American journal of translational research · 2025Article
- Exploring the causal association between uric acid and lung cancer in east Asian and European populations: a mendelian randomization study.BMC cancer · 2024Article
- The Good, the Bad and the New about Uric Acid in Cancer.Cancers · 2022Review
- Trastuzumab and Doxorubicin Sequential Administration Increases Oxidative Stress and Phosphorylation of Connexin 43 on Ser368.International journal of molecular sciences · 2022Article
- Review
- The study of correlation between nomogram prediction of uric acid and different chemotherapy regimens in breast cancer patients.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2022Article
- Xanthine Oxidoreductase-Mediated Superoxide Production Is Not Involved in the Age-Related Pathologies inInternational journal of molecular sciences · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDoxorubicin is an anthracycline antibiotic, which is effective for treating various malignancies such as leukemias and lymphomas. However, its serious cumulative dose-dependent cardiotoxicity limits its clinical application. Previous studies have shown that doxorubicin-associated cardiotoxicity is closely related to adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK). Uric acid is known to exert a strong antioxidant function and moderate protection on the nerves. However, its cardioprotective properties have not been established. This study aimed to investigate the potential effect of uric acid preconditioning on doxorubicin-induced cardiotoxicity and the involvement of AMPK signaling in this process.
methodsAn acute cardiotoxicity model of doxorubicin was established by intraperitoneal injection of a single dose of doxorubicin (20 mg/kg) in mice. Uric acid (62.5, 125, and 250 mg/kg) was intragastrically administered to mice one day before doxorubicin treatment and then continuously administered every 24 h for 8 consecutive days. The mortality rate and weight of the mice were recorded every day. Electrocardiograms (ECG) and serum biochemicals were detected with an ECG instrument and enzyme-linked immunosorbent assay kit (Elisa) respectively. A real-time cell analyzer (RTCA) was used to investigate the cytotoxicity of doxorubicin
resultsUric acid (125 mg/kg) preconditioning increased the survival rate and body weight of doxorubicin-treated mice. Uric acid also effectively alleviated prolongation of the doxorubicin-induced QT interval, slowed heart rate, and reduced the plasma levels of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK) in plasma in mice. Moreover, uric acid strongly activated AMPK and Src homology 2 domain-containing protein tyrosine phosphatase (SHP2), inhibiting doxorubicin-induced expression phosphorylated-c-Jun N-terminal kinases (JNK) and phosphorylated-connexin 43 (Cx43)
conclusionsWe demonstrated that uric acid preconditioning alleviated doxorubicin-induced cardiotoxicity through the AMPK-SHP2-JNK-Cx43 signaling pathway.
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