ArticleJournal of neuroinflammation2020
HMGB1/RAGE axis mediates stress-induced RVLM neuroinflammation in mice via impairing mitophagy flux in microglia.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 166 citations in OpenAlex.
- Morroniside maintains mitochondrial homeostasis in microglia and mitigates neuroinflammation in experimental autoimmune encephalomyelitis.Journal of neuropathology and experimental neurology · 2026Article
- Mitochondrial dysfunction in microglia: a novel perspective of depression pathogenesis.Inflammation and regeneration · 2026Review
- HMGB1 in Amyloid-Beta Pathology: Mechanistic Insights and Therapeutic Implications for Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Recent advances in methotrexate pharmacology and potential therapeutic uses in age-related cardiometabolic and neurodegenerative diseases.Pharmacological reviews · 2026Review
- HMGB1 impairs nasal epithelial barrier via regulating autophagy in the pathogenesis of allergic rhinitis.The World Allergy Organization journal · 2026Article
- Targeted biohybrid nanoplatform for spinal cord injury treatment: Restoring microglial mitophagy and alleviating oxidative stress.Materials today. Bio · 2026Article
- Central Sympathetic Nerve Activation-Mediated Hypertension: Target Mechanisms and Multimodal Interventions-From Basic Research to Clinical Translation.International journal of molecular sciences · 2026Review
- Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury.Neural regeneration research · 2026Article
- Early HMGB1 Inhibition Reduces Hippocampal Injury During Adolescence in a Young Mouse Model of Radiation-Induced Brain Injury.Cellular and molecular neurobiology · 2026Article
- The Role of Crosstalk Between the Unfolded Protein Response and Autophagy in Diseases Associated with Sympathetic Nervous System Imbalance: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Targeting microglial inflammation in Parkinson's disease: irisin activates PAFAH1B1-RAGE ubiquitination and TFEB-dependent autophagy to alleviate neurodegeneration.Communications biology · 2026Article
- Lévy statistics define anxiety and depression in mice subjected to chronic stress.Frontiers in behavioral neuroscience · 2026Article
- Central neural circuits and their associated mechanisms of inter-organ crosstalk.Frontiers in cell and developmental biology · 2026Review
- Perioperative neurocognitive disorders: Advances in molecular mechanisms and bioactive molecules.Ageing research reviews · 2025Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- PDZD8 Dysregulation Mediates RVLM Neuronal Hyperexcitation Via Activation of CaMolecular neurobiology · 2025Article
- The HMGB1-RAGE Axis Drives the Proneural-to-Mesenchymal Transition and Aggressiveness in Glioblastoma.International journal of molecular sciences · 2025Article
- Chronic Stress Induces Sex-Specific Renal Mitochondrial Dysfunction in Mice.Function (Oxford, England) · 2025Article
- Inhibition of the HMGB1-RAGE Axis Attenuates Microglial Inflammation and Ameliorates Hypoxia-Induced Cognitive Impairment.International journal of molecular sciences · 2025Article
- Mitochondrial sirtuins 3, 4 and 5 in patients with psoriasis.Immunologic research · 2025Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMicroglial mediated neuroinflammation in the rostral ventrolateral medulla (RVLM) plays roles in the etiology of stress-induced hypertension (SIH). It was reported that autophagy influenced inflammation via immunophenotypic switching of microglia. High-mobility group box 1 (HMGB1) acts as a regulator of autophagy and initiates the production of proinflammatory cytokines (PICs), but the underlying mechanisms remain unclear.
methodsThe stressed mice were subjected to intermittent electric foot shocks plus noises administered for 2 h twice daily for 15 consecutive days. In mice, blood pressure (BP) and renal sympathetic nerve activity (RSNA) were monitored by noninvasive tail-cuff method and platinum-iridium electrodes placed respectively. Microinjection of siRNA-HMGB1 (siHMGB1) into the RVLM of mice to study the effect of HMGB1 on microglia M1 activation was done. mRFP-GFP-tandem fluorescent LC3 (tf-LC3) vectors were transfected into the RVLM to evaluate the process of autolysosome formation/autophagy flux. The expression of RAB7, lysosomal-associated membrane protein 1 (LAMP1), and lysosomal pH change were used to evaluate lysosomal function in microglia. Mitophagy was identified by transmission electron microscopic observation or by checking LC3 and MitoTracker colocalization under a confocal microscope.
resultsWe showed chronic stress increased cytoplasmic translocations of HMGB1 and upregulation of its receptor RAGE expression in microglia. The mitochondria injury, oxidative stress, and M1 polarization were attenuated in the RVLM of stressed Cre-CX3CR1/RAGE
conclusionsCollectively, we demonstrated that inhibition of the HMGB1/RAGE axis activation led to increased stress-induced mitophagy flux, hence reducing the activity of microglia-mediated neuroinflammation and consequently reduced the sympathetic vasoconstriction drive in the RVLM.
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Registered trials
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.