Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia

Abstract This study investigated the roles and mechanisms of PINK1 activity in neonatal hypoxia-induced seizures with shRNA intervention targeting translocase outer mitochondrial membrane 7 (TOM7), the positive regulator of PINK1 autophosphorylation, or overlapping with the m-AAA protease 1 homolog...

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Main Authors: Yi Yuan, Xiaoqian Wang, Yaru Cui, Hua Zhou, Wenna Li, Qian Teng, Hongjin Wang, Bohan Sun, Qiaoyun Wang, Hongliu Sun, Jianhua Tang
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-99915-8
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author Yi Yuan
Xiaoqian Wang
Yaru Cui
Hua Zhou
Wenna Li
Qian Teng
Hongjin Wang
Bohan Sun
Qiaoyun Wang
Hongliu Sun
Jianhua Tang
author_facet Yi Yuan
Xiaoqian Wang
Yaru Cui
Hua Zhou
Wenna Li
Qian Teng
Hongjin Wang
Bohan Sun
Qiaoyun Wang
Hongliu Sun
Jianhua Tang
author_sort Yi Yuan
collection DOAJ
description Abstract This study investigated the roles and mechanisms of PINK1 activity in neonatal hypoxia-induced seizures with shRNA intervention targeting translocase outer mitochondrial membrane 7 (TOM7), the positive regulator of PINK1 autophosphorylation, or overlapping with the m-AAA protease 1 homolog (OMA1), the negative regulator of PINK1 autophosphorylation. Studies have suggested that in hypoxia-induced neonatal seizures, the phosphorylation level of PINK1 is significantly increased and the mitophagic pathway is activated, accompanied by neuronal damage and learning-memory deficits. Inhibiting PINK1 phosphorylation by reducing TOM7 expression alleviated mitophagy, mitochondrial oxidative stress, neuronal damage and seizures. In contrast, the inhibition of OMA1 expression resulted in a further increase in PINK1 phosphorylation and aggravated hypoxia-induced seizures and neuronal injury. This study implicated PINK1 activity in neonatal hypoxia and suggest that attenuated PINK1 autophosphorylation may have neuroprotective and anti-seizure effects in neonatal hypoxia.
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issn 2045-2322
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publishDate 2025-04-01
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series Scientific Reports
spelling doaj-art-5a2c3497d0854f4e8dc399fea1b856cd2025-08-20T02:10:50ZengNature PortfolioScientific Reports2045-23222025-04-0115111510.1038/s41598-025-99915-8Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxiaYi Yuan0Xiaoqian Wang1Yaru Cui2Hua Zhou3Wenna Li4Qian Teng5Hongjin Wang6Bohan Sun7Qiaoyun Wang8Hongliu Sun9Jianhua Tang10School of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversityAffiliated Yantai Mountain Hospital, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversitySchool of Pharmaceutical Sciences, Binzhou Medical UniversityAffiliated Yantai Mountain Hospital, Binzhou Medical UniversityAbstract This study investigated the roles and mechanisms of PINK1 activity in neonatal hypoxia-induced seizures with shRNA intervention targeting translocase outer mitochondrial membrane 7 (TOM7), the positive regulator of PINK1 autophosphorylation, or overlapping with the m-AAA protease 1 homolog (OMA1), the negative regulator of PINK1 autophosphorylation. Studies have suggested that in hypoxia-induced neonatal seizures, the phosphorylation level of PINK1 is significantly increased and the mitophagic pathway is activated, accompanied by neuronal damage and learning-memory deficits. Inhibiting PINK1 phosphorylation by reducing TOM7 expression alleviated mitophagy, mitochondrial oxidative stress, neuronal damage and seizures. In contrast, the inhibition of OMA1 expression resulted in a further increase in PINK1 phosphorylation and aggravated hypoxia-induced seizures and neuronal injury. This study implicated PINK1 activity in neonatal hypoxia and suggest that attenuated PINK1 autophosphorylation may have neuroprotective and anti-seizure effects in neonatal hypoxia.https://doi.org/10.1038/s41598-025-99915-8PINK1MitophagySeizureNeuronal injuryMitochondrial oxidative stress
spellingShingle Yi Yuan
Xiaoqian Wang
Yaru Cui
Hua Zhou
Wenna Li
Qian Teng
Hongjin Wang
Bohan Sun
Qiaoyun Wang
Hongliu Sun
Jianhua Tang
Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
Scientific Reports
PINK1
Mitophagy
Seizure
Neuronal injury
Mitochondrial oxidative stress
title Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
title_full Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
title_fullStr Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
title_full_unstemmed Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
title_short Attenuated PINK1 autophosphorylation play neuroprotective and anti-seizure roles in neonatal hypoxia
title_sort attenuated pink1 autophosphorylation play neuroprotective and anti seizure roles in neonatal hypoxia
topic PINK1
Mitophagy
Seizure
Neuronal injury
Mitochondrial oxidative stress
url https://doi.org/10.1038/s41598-025-99915-8
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