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<p>Recent studies in cardiac biology have identified a complex interplay between the Hippo, Wnt/β-catenin, and Notch signaling pathways, establishing an integrated regulatory network that influences cardiac growth and function. Deletion of MST1/2 activates the YAP/TAZ, STAT3, Wnt/β-catenin, and Notch pathways, highlighting the key role of YAP/TAZ in facilitating the crosstalk of these pathways. Activation of the Wnt/β-catenin pathway inhibits the positive feedback loop between Notch signaling and YAP/TAZ, elucidating the dynamic balance of these signaling systems. Communication between YAP and β-catenin in the nucleus regulates the expression of genes associated with cell proliferation and reprogramming, including <i>Sox2</i> and <i>Snai2</i>. Although YAP forms a complex with the transcription factors TEAD/TEF while β-catenin with LEF/TCF, the two pathways exhibit distinct regulatory functions with partial overlap in gene targets. The Hippo pathway regulates heart size and cardiomyocyte proliferation by inhibiting Wnt/β-catenin signaling. Disruption of this balance can result in aberrant cardiac development and associated diseases, highlighting the need for a thorough understanding of these interactions. Therapeutics targeting of these signaling pathways have the potential to impact cardiac development and repair, creating new treatment options for heart disease.</p>

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Crosstalk between MST1-Hippo and Wnt/β-Catenin, Notch, and PI3K/Akt pathways in cardiac physiology and pathology

  • 期刊论文

  • 发表日期：

    2025年6月9日

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  • Jin Wang,
  • Kai Jing,
  • Vadim Mitrokhin,
  • Stanislav Schileyko,
  • Anastasija Rodina,
  • Alexandra Zolotareva,
  • Valentin Zolotarev,
  • Natalia Bocharnikova,
  • Dmitry Kaminer,
  • Emilija Antova,
  • Radoslav Stojchevski,
  • Nikola Hadzi-Petrushev,
  • Dimiter Avtanski,
  • Andre Kamkin,
  • Mitko Mladenov

摘要

Recent studies in cardiac biology have identified a complex interplay between the Hippo, Wnt/β-catenin, and Notch signaling pathways, establishing an integrated regulatory network that influences cardiac growth and function. Deletion of MST1/2 activates the YAP/TAZ, STAT3, Wnt/β-catenin, and Notch pathways, highlighting the key role of YAP/TAZ in facilitating the crosstalk of these pathways. Activation of the Wnt/β-catenin pathway inhibits the positive feedback loop between Notch signaling and YAP/TAZ, elucidating the dynamic balance of these signaling systems. Communication between YAP and β-catenin in the nucleus regulates the expression of genes associated with cell proliferation and reprogramming, including Sox2 and Snai2. Although YAP forms a complex with the transcription factors TEAD/TEF while β-catenin with LEF/TCF, the two pathways exhibit distinct regulatory functions with partial overlap in gene targets. The Hippo pathway regulates heart size and cardiomyocyte proliferation by inhibiting Wnt/β-catenin signaling. Disruption of this balance can result in aberrant cardiac development and associated diseases, highlighting the need for a thorough understanding of these interactions. Therapeutics targeting of these signaling pathways have the potential to impact cardiac development and repair, creating new treatment options for heart disease.