ArticleAnnals of clinical and translational neurology2021
PINK1 antagonize intracerebral hemorrhage by promoting mitochondrial autophagy.
Article in Annals of clinical and translational neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Microglial Mitochondrial Dysfunction: The Storm Center of Post-Stroke Neuroinflammation.CNS neuroscience & therapeutics · 2026Review
- Organelle regulation of ferroptosis after intracerebral hemorrhage.Redox biology · 2026Review
- Autophagy in ischemic stroke: from cellular survival mechanism to pathological damage.Metabolic brain disease · 2026Review
- Mitochondrial dysfunction in intracerebral hemorrhage: molecular mechanisms and pathological consequences.Frontiers in cellular neuroscience · 2026Review
- Mitochondrial dysfunction and PANoptosis-related signaling in acute central nervous system injuries: mechanistic convergence and therapeutic opportunities.Frontiers in molecular neuroscience · 2026Review
- Mitochondrial Quality Control: Insights into Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2025Review
- Longitudinal change and prognostic significance of serum PINK1 levels, and mediation role of delayed cerebral ischemia in human aneurysmal subarachnoid hemorrhage: an observational analytical study.Frontiers in neurology · 2025Article
- Aging and Autophagy: Roles in Musculoskeletal System Injury.Aging and disease · 2024Review
- Signature and function of plasma exosome-derived circular RNAs in patients with hypertensive intracerebral hemorrhage.Molecular genetics and genomics : MGG · 2024Article
- Pink1 deficiency enhances neurological deficits and inflammatory responses after intracerebral hemorrhage in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.Neural regeneration research · 2024Review
- Review
- The use of multiple datasets to identify autophagy-related molecular mechanisms in intracerebral hemorrhage.Frontiers in genetics · 2023Article
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
- Microglial autophagy in cerebrovascular diseases.Frontiers in aging neuroscience · 2022Review
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracerebral hemorrhage (ICH) causes neurotransmitter release, oligemia, membrane depolarization, mitochondrial dysfunction, and results in the high rate of mortality and functional disability. Here, we focus on PTEN-induced kinase 1 (PINK1), a mitochondrial-targeted protein kinase, and explore its role in ICH progression.
methodsThe qPCR and Western blot were performed to examine the expression of PINK1 in ICH patients and mouse model. PINK1 gain- and loss-of-function mice were used to evaluate their protective role on brain injury and behavioral disorders. Flow cytometry was carried out, mitochondrial membrane potential and reactive oxygen species production were detected to explore the distribution and neuroprotective function of PINK1.
resultsPINK1 mRNA was upregulated, however, its protein was downregulated in ICH patients. The reduction of PINK1 was mainly happened in microglial cells in ICH model. Overexpression of PINK1 is able to rescue ICH-induced behavioral disorders. PINK1 protects ICH-induced brain injury by promoting mitochondrial autophagy in microglia.
conclusionPINK1 possesses a neuroprotective role and antagonizes ICH by promoting mitochondrial autophagy, which may be of value as a therapeutic target for ICH treatment.
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