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Background <p>Endothelial dysfunction is considered to play a pivotal role in the pathogenesis of preeclampsia (PE). Transcutaneous auricular vagus nerve stimulation (taVNS) is a potential non-pharmaceutical alternative treatment for PE. This study aimed to explore the mechanisms of taVNS on endothelial dysfunction.</p> Methods <p>We used the reduced uterine perfusion pressure method to establish PE model and TNF-α to establish endothelial dysfunction model in HUVECs. In vivo, we detected blood pressure, vascular proteomics and morphology, ACh and receptor α7nAChR, and inflammatory factors (IL-6, IL-1β, and TNF-α). In vitro, we checked cell viability, mitochondrial membrane potential, apoptosis rate, calcium levels, HUVECs morphology, and Endoplasmic reticulum (ER) and mitochondria (MITO) interaction.</p> Results <p>taVNS promoted the release of ACh, which decreased Ca<sup>2+</sup> inflow from ER to MITO through the IP3R1/GRP75/VDAC1 complex, presumably through α7nAChR. This reduced the release of pro-apoptotic proteins (cleaved caspase-3, HSC70, and cytochrome C) and helped preserve the morphological and functional integrity of mitochondria, thus reducing the apoptosis of HUVECs, improving endothelial function, and relieving PE.</p> Conclusion <p>taVNS may exert an anti-PE effect through ER-MITO interaction. These findings offer preliminary insights into PE pathogenesis, and suggest that the ACh/α7nAChR axis and IP3R1/GRP75/VDAC1 complex could be promising targets for future therapeutic investigation.</p>

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taVNS alleviates preeclampsia-induced vascular endothelial dysfunction via α7nAChR- IP3R1/GRP75/VDAC1 signal pathway

  • 期刊论文

  • 发表日期：

    2025年9月23日

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  • Jing Zhao,
  • Yuman Lei,
  • Chengcheng Mu,
  • Yuwei Wu,
  • Rourou Fang,
  • Dongdong Wu,
  • Shouzhu Xu,
  • Haifa Qiao

摘要

Background

Endothelial dysfunction is considered to play a pivotal role in the pathogenesis of preeclampsia (PE). Transcutaneous auricular vagus nerve stimulation (taVNS) is a potential non-pharmaceutical alternative treatment for PE. This study aimed to explore the mechanisms of taVNS on endothelial dysfunction.

Methods

We used the reduced uterine perfusion pressure method to establish PE model and TNF-α to establish endothelial dysfunction model in HUVECs. In vivo, we detected blood pressure, vascular proteomics and morphology, ACh and receptor α7nAChR, and inflammatory factors (IL-6, IL-1β, and TNF-α). In vitro, we checked cell viability, mitochondrial membrane potential, apoptosis rate, calcium levels, HUVECs morphology, and Endoplasmic reticulum (ER) and mitochondria (MITO) interaction.

Results

taVNS promoted the release of ACh, which decreased Ca2+ inflow from ER to MITO through the IP3R1/GRP75/VDAC1 complex, presumably through α7nAChR. This reduced the release of pro-apoptotic proteins (cleaved caspase-3, HSC70, and cytochrome C) and helped preserve the morphological and functional integrity of mitochondria, thus reducing the apoptosis of HUVECs, improving endothelial function, and relieving PE.

Conclusion

taVNS may exert an anti-PE effect through ER-MITO interaction. These findings offer preliminary insights into PE pathogenesis, and suggest that the ACh/α7nAChR axis and IP3R1/GRP75/VDAC1 complex could be promising targets for future therapeutic investigation.