ArticleAnnals of translational medicine2021
BMAL1 attenuates intracerebral hemorrhage-induced secondary brain injury in rats by regulating the Nrf2 signaling pathway.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- A Systematic Review of MicroRNAs in Hemorrhagic Neurovascular Disease: Cerebral Cavernous Malformations as a Paradigm.International journal of molecular sciences · 2025Pooled it
- Exercise and Circadian Rhythm Regulation: Mechanisms, Resilience, and Therapeutic Potential for Neurological Diseases.CNS neuroscience & therapeutics · 2026Review
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- From bench to bedside: nanomedicine development for intracerebral hemorrhage - exploring microenvironment, innovation, and translation.Journal of nanobiotechnology · 2025Review
- Article
- miRNA506 Activates Sphk1 Binding with Sirt1 to Inhibit Brain Injury After Intracerebral Hemorrhage via PI3K/AKT Signaling Pathway.Molecular neurobiology · 2025Article
- Clinical Implication of Time of Ischaemic Stroke Among Post-Stroke Survivors from Eastern India: A Circadian Perspective.Neuromolecular medicine · 2024Article
- Impact of circadian clock protein Bmal1 on experimentally-induced periodontitis-associated renal injury.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024Article
- miR-155-5p/Bmal1 Modulates the Senescence and Osteogenic Differentiation of Mouse BMSCs through the Hippo Signaling Pathway.Stem cell reviews and reports · 2024Article
- Neuroinflammation and iron metabolism after intracerebral hemorrhage: a glial cell perspective.Frontiers in neurology · 2024Review
- Establishment of a rat model of severe spontaneous intracerebral hemorrhage.Journal of intensive medicine · 2024Article
- Role and regulatory mechanism of microRNA mediated neuroinflammation in neuronal system diseases.Frontiers in immunology · 2023Review
- The time dimension to stroke: Circadian effects on stroke outcomes and mechanisms.Neurochemistry international · 2023Article
- MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy.Frontiers in immunology · 2022Review
- Regulation of nuclear factor erythroid-2-related factor 2 as a potential therapeutic target in intracerebral hemorrhage.Frontiers in molecular neuroscience · 2022Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracerebral hemorrhage (ICH) is a severe cerebrovascular disease with high morbidity and mortality rates. Oxidative stress and inflammation are important pathological mechanisms of secondary brain injury (SBI) after ICH. Brain and muscle Arnt-like protein 1 (BMAL1), which forms the core component of the circadian clock, was previously shown to be involved in many diseases and to participate in oxidative stress and inflammatory responses. However, the role of BMAL1 in SBI following ICH is unknown. In addition, treatments targeting miR-155 and its downstream signaling pathway may exert a beneficial effect on SBI after ICH, while miR-155 may regulate Bmal1 mRNA stability and translation. Nevertheless, researchers have not clearly determined whetheantagomir-155 upregulates BMAL1 expression and subsequently attenuates ICH-induced brain injury in rats.
methodsAfter establishing an ICH rat model by injecting autologous blood, the time course of changes in levels of the BMAL1 protein after ICH was analyzed. Subsequently, this study was designed to investigate the potential role and mechanisms of BMAL1 in SBI following ICH using lentiviral overexpression and antagomir-155 treatments.
resultsBMAL1 protein levels were significantly decreased in the ICH group compared to the sham group. Genetic overexpression of BMAL1 alleviated oxidative stress, inflammation, brain edema, blood-brain barrier injury, neuronal death, and neurological dysfunction induced by ICH. On the other hand, we observed that inhibiting miRNA-155 using antagomir-155 promoted the expression of BMAL1 and further activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway to attenuate brain injury after ICH.
conclusionsThese results reveal that BMAL1 serves as a neuroprotective agent in ICH and upregulation of BMAL1 attenuates ICH-induced SBI. Therefore, BMAL1 may be a promising therapeutic target for SBI following ICH.
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