ArticleAging cell2021
Microglial MT1 activation inhibits LPS-induced neuroinflammation via regulation of metabolic reprogramming.
Article in Aging cell, 2021. 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 55 papers.
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Who cites it
55 citing papers in PubMed, 94 citations in OpenAlex.
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- The spatiotemporal dynamic evolution of post-stroke neuroinflammation: energy metabolism mechanisms of acute response and chronic progression.Frontiers in pharmacology · 2026Review
- Acupuncture regulates neuroinflammation: microglial glucose metabolism reprogramming as a potential mediating mechanism.Frontiers in immunology · 2026Review
- Cuproptosis: A Potential Target for the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2026Review
- Melatonin orchestrates mitochondrial fusion dynamics-mediated WNT/β-catenin signaling to promote dopaminergic neuronal differentiation of human iPS and nerve regeneration in a MPTP-induced mouse model of Parkinson's disease.Cell death discovery · 2025Article
- Baicalein alleviates long-term cognitive impairments induced by repeated neonatal sevoflurane exposure via inhibition of cortical microglial TLR4/NF-kB signaling.Brain, behavior, & immunity - health · 2025Article
- High-throughput cytokine detection platform for evaluation of chemical induced microglial activation.SLAS technology · 2025Article
- Regulation of mitochondrial dynamics and function by melatonin type 1 receptor in parkinson's disease.Cellular and molecular life sciences : CMLS · 2025Article
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- Characterization of SPTLC2 as a key driver promoting microglial activation and energy metabolism reprogramming after ischemic stroke through bulk and single-cell analyses combined with experimental validation.Cell biology and toxicology · 2025Article
- NG-497 Alleviates Microglia-Mediated Neuroinflammation in a MTNR1A-Dependent Manner.Inflammation · 2025Article
- THSG counteracts microglial glycolytic reprogramming and neuronal necroptosis both in vivo and in vitro under conditions of neuroinflammation.Scientific reports · 2025Article
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- Dapagliflozin Improves High-Fat Diet-Induced Cognitive Impairment in Female Mice.Brain and behavior · 2025Article
- PKR modulates sterile systemic inflammation-triggered neuroinflammation and brain glucose metabolism disturbances.Frontiers in immunology · 2025Article
- Glycolytic reprogramming during microglial polarization in neurological diseases.Frontiers in immunology · 2025Review
- Effects of Melatonin Disorders on Parkinson's Disease: A Review of Mechanisms and Clinical Manifestations.Neuropsychiatric disease and treatment · 2025Review
- Ramelteon exposure and survival of critically Ill sepsis patients: a retrospective study from MIMIC-IV.BMC anesthesiology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia-mediated neuroinflammation makes a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN). Neuronal MT1 is a neuroprotective factor, but it remains largely unknown whether dysfunction of microglial MT1 is involved in the PD pathogenesis. Here, we found that MT1 was reduced in microglia of SN in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. Microglial MT1 activation dramatically inhibited lipopolysaccharide (LPS)-induced neuroinflammation, whereas loss of microglial MT1 aggravated it. Metabolic reprogramming of microglia was found to contribute to the anti-inflammatory effects of MT1 activation. LPS-induced excessive aerobic glycolysis and impaired oxidative phosphorylation (OXPHOS) could be reversed by microglial MT1 activation. MT1 positively regulated pyruvate dehydrogenase alpha 1 (PDHA1) expression to enhance OXPHOS and suppress aerobic glycolysis. Furthermore, in LPS-treated microglia, MT1 activation decreased the toxicity of conditioned media to the dopaminergic (DA) cell line MES23.5. Most importantly, the anti-inflammatory effects of MT1 activation were observed in LPS-stimulated mouse model. In general, our study demonstrates that MT1 activation inhibits LPS-induced microglial activation through regulating its metabolic reprogramming, which provides a mechanistic insight for microglial MT1 in anti-inflammation.
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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.