ArticleJournal of neuroinflammation2019
Cathepsin C promotes microglia M1 polarization and aggravates neuroinflammation via activation of Ca
Article in Journal of neuroinflammation, 2019. 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 75 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 127 citations in OpenAlex.
- Inhibition of Cathepsin C attenuates osteoarthritis by modulating macrophage activated status and reducing tissue inflammatory responses.Bone & joint research · 2026Article
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- Compatibility of Acorus tatarinowii Schott and Polygala tenuifolia Willd. alleviate Alzheimer's disease through regulating Nos2-mediated calcium signaling pathway.Neurochemical research · 2026Article
- O-GlcNAcylation regulates microglial neuroinflammation in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- Precision acupuncture for chemotherapy-induced peripheral neuropathy: multitarget mechanisms and integrated clinical translation framework.Frontiers in neurology · 2026Review
- The effect of neuroimmune signalling on drug addiction.Frontiers in pharmacology · 2026Review
- Cystatin F as a neuroimmune effector in CNS inflammation and neurodegeneration.Frontiers in cell and developmental biology · 2026Review
- Ultra-processed foods sourced 7-ketositosterol aggravates colitis through gut dysbiosis induced-PDLIM3 activation.Gut microbes · 2025Article
- Smart nanovehicles crossing the barricade: precision targeting of neuroinflammation for ischemic stroke diagnostics and therapeutics.Journal of nanobiotechnology · 2025Review
- Targeting Cathepsins in Neurodegeneration: Biochemical Advances.Biomedicines · 2025Review
- Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Piezo1 exacerbates psoriasis by promoting macrophage M1 polarization and inhibits autophagy via activating PI3K/AKT signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025Review
- GDF11 Mitigates Neuropathic Pain via Regulation of Microglial Polarization and Neuroinflammation through TGF-βR1/SMAD2/NF-κB Pathway in Male Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- TRIM14 Inhibition Suppresses Microglial Polarization and Pyroptosis Through the NF-κB/NLRP3 Pathway to Enhance Spinal Cord Injury Repair.Mediators of inflammation · 2025Article
- Regulatory Mechanisms and Therapeutic Implications of Lysosomal Dysfunction in Alzheimer's Disease.International journal of biological sciences · 2025Review
- Protective Role of Electroacupuncture Against Cognitive Impairment in Neurological Diseases.Current neuropharmacology · 2025Review
- The multifaceted roles of cathepsins in immune and inflammatory responses: implications for cancer therapy, autoimmune diseases, and infectious diseases.Biomarker research · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundMicroglia-derived lysosomal cathepsins are important inflammatory mediators to trigger signaling pathways in inflammation-related cascades. Our previous study showed that the expression of cathepsin C (CatC) in the brain is induced predominantly in activated microglia in neuroinflammation. Moreover, CatC can induce chemokine production in brain inflammatory processes. In vitro studies further confirmed that CatC is secreted extracellularly from LPS-treated microglia. However, the mechanisms of CatC affecting neuroinflammatory responses are not known yet.
methodsCatC over-expression (CatCOE) and knock-down (CatCKD) mice were treated with intraperitoneal and intracerebroventricular LPS injection. Morris water maze (MWM) test was used to assess the ability of learning and memory. Cytokine expression in vivo was detected by in situ hybridization, quantitative PCR, and ELISA. In vitro, microglia M1 polarization was determined by quantitative PCR. Intracellular Ca
resultsThe LPS-treated CatCOE mice exhibited significantly increased escape latency compared with similarly treated wild-type or CatCKD mice. The highest levels of TNF-α, IL-1β, and other M1 markers (IL-6, CD86, CD16, and CD32) were found in the brain or serum of LPS-treated CatCOE mice, and the lowest levels were detected in CatCKD mice. Similar results were found in LPS-treated microglia derived from CatC differentially expressing mice or in CatC-treated microglia from wild-type mice. Furthermore, the expression of NR2B mRNA, phosphorylation of NR2B, Ca
conclusionThe data suggest that CatC promotes microglia M1 polarization and aggravates neuroinflammation via activation of Ca
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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.