HIPK2 protects neurons from oxidative stress and modulates central nervous system responses following traumatic brain injury.

Authors

Qiangbin Zhu, Fan Wang, Bojun Zhang, Zhigang Pan, Xiaodong Kang, Weipeng Hu

Published in

Iranian journal of basic medical sciences. Volume 29. Issue 5. Pages 804-811.

Abstract

Traumatic brain injury (TBI) induces oxidative stress, contributing to secondary neuronal damage. This study aimed to elucidate the role of the stress-responsive kinase HIPK2 in regulating endogenous antioxidant defenses in neural tissue following TBI.
We employed complementary in vitro and in vivo models: an H₂O₂-induced oxidative stress model in PC12 cells (with HIPK2 inhibited by tBID) and a controlled cortical impact mouse model of TBI (with HIPK2 overexpressed via intracerebroventricular Ad-HIPK2 injection). Analyses included assessments of cell viability, mRNA expression, and protein levels of key antioxidant factors (HO-1, UGT1A1, NQO1).
In vitro, HIPK2 inhibition markedly increased oxidative stress-induced cell death and significantly down-regulated UGT1A1 expression. In vivo, endogenous HIPK2 expression was significantly suppressed post-TBI. Conversely, HIPK2 overexpression effectively rescued the expression of antioxidant proteins UGT1A1 and NQO1.
These results demonstrate that HIPK2 is a critical modulator of the antioxidant response after TBI, capable of orchestrating key defense genes and conferring neuroprotection. Our findings identify HIPK2 as a promising molecular target for therapeutic intervention against TBI-related oxidative damage.

PMID:
42291397
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.

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