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Backgroud <p>Hyperthyroid heart disease (HHD) is characterized by cardiac remodeling and inflammation, yet targeted therapies remain limited. LCZ696 (sacubitril/valsartan) has demonstrated cardioprotective effects, but its mechanisms in HHD are unclear.</p> Methods <p>In this study, Network pharmacology alongside experimental validation were employed to elucidate the pharmacological mechanisms of LCZ696 in the treatment of HHD. We identified potential targets for LCZ696 and relevant HHD-related genes from public databases. The mechanisms by which LCZ696 exerts its effects on HHD were further elucidated through GO, KEGG and PPI analysis. The potential molecular targets of LCZ696 were evaluated by molecular docking. Additionally, Echocardiography-measured cardiac function, myocardial fibrosis, target Genes and Inflammatory responses of cardiomyocytes in rat were also examined.</p> Results <p>A total of 78 target genes for LCZ696 and 1520 HHD targets were obtained. 35 overlapping genes were determined as potential targets of LCZ696 in treating HHD. The PPI analyses highlighted targets being associated with HHD as STAT3, STAT1 and MUC1, suggesting potential binding interactions with LCZ696, as verified by molecular docking analysis, which were also consistent with the experimental results.</p> Conclusions <p>LCZ696 may ameliorate HHD, potentially associated with reduced inflammation and downregulation of STAT3 signaling.</p> Graphical Abstract <p></p>

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The potential mechanisms of LCZ696 for anti-hyperthyroid heart disease: an integrative approach of network pharmacology, molecular docking and in vivo verification

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月30日

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  • Xianghui Zeng,
  • Lihua Wen,
  • Luoying Liu,
  • Qingfeng Zeng,
  • Jianping Luo

摘要

Backgroud

Hyperthyroid heart disease (HHD) is characterized by cardiac remodeling and inflammation, yet targeted therapies remain limited. LCZ696 (sacubitril/valsartan) has demonstrated cardioprotective effects, but its mechanisms in HHD are unclear.

Methods

In this study, Network pharmacology alongside experimental validation were employed to elucidate the pharmacological mechanisms of LCZ696 in the treatment of HHD. We identified potential targets for LCZ696 and relevant HHD-related genes from public databases. The mechanisms by which LCZ696 exerts its effects on HHD were further elucidated through GO, KEGG and PPI analysis. The potential molecular targets of LCZ696 were evaluated by molecular docking. Additionally, Echocardiography-measured cardiac function, myocardial fibrosis, target Genes and Inflammatory responses of cardiomyocytes in rat were also examined.

Results

A total of 78 target genes for LCZ696 and 1520 HHD targets were obtained. 35 overlapping genes were determined as potential targets of LCZ696 in treating HHD. The PPI analyses highlighted targets being associated with HHD as STAT3, STAT1 and MUC1, suggesting potential binding interactions with LCZ696, as verified by molecular docking analysis, which were also consistent with the experimental results.

Conclusions

LCZ696 may ameliorate HHD, potentially associated with reduced inflammation and downregulation of STAT3 signaling.

Graphical Abstract