ArticleNeurochemical research2024
NL-1 Promotes PINK1-Parkin-Mediated Mitophagy Through MitoNEET Inhibition in Subarachnoid Hemorrhage.
Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Medicinal Chemistry Review of the NEET Protein Family.ChemMedChem · 2026Review
- Gram-scale synthesis of the thiazolidinedione-based mitoNEET ligand NL-1 using a Hantzsch ester reduction.Tetrahedron letters · 2026Article
- Iron-driven secondary injury after intracranial hemorrhage: mitochondrial dysfunction and ferroptosis.Frontiers in neuroscience · 2026Review
- Exploring CISD1 as a multifaceted biomarker in cancer: Implications for diagnosis, prognosis, and immunotherapeutic response.Genes & diseases · 2025Article
- Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.Molecular neurobiology · 2025Review
- Loss of the mitochondrial protein mitoNEET in mice is associated with cognitive impairments and increased neuroinflammation.Journal of Alzheimer's disease : JAD · 2025Article
- Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review.Cellular and molecular neurobiology · 2024Review
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
- NAD-Dependent Protein Deacetylase Sirtuin-1 Mediated Mitophagy Regulates Early Brain Injury After Subarachnoid Hemorrhage.Journal of inflammation research · 2024Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
NL-1 is a mitoNEET ligand known for its antileukemic effects and has recently shown neuroprotective effects in an ischemic stroke model. However, its underlying process in subarachnoid hemorrhage (SAH) is still unclear. Thus, we aimed to investigate the possible mechanism of NL-1 after SAH in rats. 112 male adult Sprague-Dawley rats were used for experiments. SAH model was performed with endovascular perforation. Rats were dosed intraperitoneally (i.p.) with NL-1 (3 mg/kg, 10 mg/kg, 30 mg/kg) or a vehicle (10% DMSO aqueous solution) at 1 h after SAH. A novel mitophagy inhibitor liensinine (60 mg/kg) was injected i.p. 24 h before SAH. SAH grades, short-term and long-term neurological scores were measured for neurobehavior. TdTmediated dUTP nick end labeling (TUNEL) staining, dihydroethidium (DHE) staining and western blot measurements were used to detect the outcomes and mechanisms of NL-1 administration. NL-1 treatment significantly improved short-term neurological behavior in Modified Garcia and beam balance sores in comparison with SAH + vehicle group. NL-1 administration also increased mitoNEET which induced phosphatase and tensin-induced kinase 1 (PINK1), Parkin and LC3II related mitophagy compared with SAH + vehicle group. In addition, the expressions of apoptotic protein Cleaved Caspase-3 and oxidative stress related protein Romo1 in NL-1 treatment group were reversed from SAH + vehicle group. Meanwhile, NL-1 treatment notably reduced TUNEL-positive cells, DHE-positive cells compared with SAH + vehicle group. NL-1 treatment notably improved long-term neurological behavior in rotarod and water maze tests compared to SAH + vehicle group. However, the administration of liensinine may inhibit the treatment effect of NL-1, leading to reduced expression of mitophagy markers Pink1, Parkin, LC3I/II, and increased expressions of Romo1 and Cleaved Caspase-3. NL-1 induced PINK1/PARKIN related mitophagy via mitoNEET, which reduced oxidative stress and apoptosis in early brain injury after SAH in rats. NL-1 may serve as a prospective drug for the treatment of SAH.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.