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CircHIPK3 regulates TGF-β1/smad3 signaling in communicating hydrocephalus after intraventricular hemorrhage by

Yexin Yuan1, Qian Ouyang2, Yijian Yang1

  • 1Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China; Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China; Hunan International Scientific and Technological Cooperation Base of Brain Tumor Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan 410008, PR China.

Brain Research Bulletin
|January 30, 2026
PubMed

Insights

Circular RNA homeodomain interacting protein kinase 3 (circHIPK3) is upregulated after intraventricular hemorrhage (IVH). Targeting circHIPK3 may treat communicating hydrocephalus by reducing fibrosis and improving neurological function.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Neurological disorders are linked to circular RNAs (circRNAs).
  • Mechanisms of circRNAs in post-intraventricular hemorrhage (IVH) communicating hydrocephalus are unclear.
  • Communicating hydrocephalus can arise after IVH, leading to neurological deficits.

Purpose of the Study:

  • Investigate the role of circHIPK3 in IVH-induced communicating hydrocephalus.
  • Elucidate the molecular mechanism of circHIPK3 in this condition.
  • Determine if circHIPK3 is a potential therapeutic target.

Main Methods:

  • Utilized IVH rat models and thrombin-induced astrocyte cell lines.
  • Assessed circHIPK3 expression levels in meningeal tissues.
  • Performed circHIPK3 knockdown experiments.
  • Analyzed fibrotic markers, ventricular size, and neurological function.
  • Investigated the interaction between circHIPK3, miR-30a-3p, ACT1, and TGF-β1/Smad3 signaling.

Main Results:

  • circHIPK3 was significantly upregulated in IVH rat meningeal tissues.
  • circHIPK3 knockdown attenuated meningeal fibrosis, reduced ventricular dilation, and improved neurological function.
  • Mechanistically, circHIPK3 sponges miR-30a-3p, upregulating ACT1 and activating TGF-β1/Smad3 signaling, promoting fibrosis.

Conclusions:

  • circHIPK3 plays a critical role in the pathogenesis of IVH-induced communicating hydrocephalus.
  • The circHIPK3/miR-30a-3p/ACT1/TGF-β1 pathway drives fibrotic progression post-IVH.
  • circHIPK3 represents a promising therapeutic target for post-IVH communicating hydrocephalus.

Keywords:
ACT1CircHIPK3FibrosisMiR-30a-3pPost-hemorrhagic hydrocephalusTGF-β1/smad3 signaling pathway

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