ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Microglial cathepsin B contributes to the initiation of peripheral inflammation-induced chronic pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Pyroptosis in Peripheral Neuropathy: From Molecular Mechanisms to Therapeutic Targeting.CNS neuroscience & therapeutics · 2026Pooled it
- Protective anti-fibrotic effect of liraglutide and Pirfenidone combination therapy on liver fibrosis in rats: effects on autophagy and NLRP3 inflammasome.BMC gastroenterology · 2025Article
- MINPP1 promotes ferroptosis in HBV-related hepatocellular carcinoma by regulating CTSB K33-linked deubiquitination via ZRANB1.Biology direct · 2025Article
- Cathepsin B deficiency disrupts cortical development via PEG3, leading to depression-like behavior.Communications biology · 2025Article
- A complex role of chromogranin A and its peptides in inflammation, autoimmunity, and infections.Frontiers in immunology · 2025Review
- Identification of Regulatory Elements in Primary Sensory Neurons Involved in Trauma-Induced Neuropathic Pain.Molecular neurobiology · 2024Article
- In vivo imaging of cathepsin B in activated glia in the brain after orofacial formalin test.Scientific reports · 2024Article
- Human β-Defensin 3 Inhibition ofCells · 2024Article
- Microglia: roles and genetic risk in Parkinson's disease.Frontiers in neuroscience · 2024Review
- Single-cell RNA-seq uncovers novel metabolic functions of Schwann cells beyond myelination.Journal of neurochemistry · 2023Article
- Identification of Cathepsin B as a Therapeutic Target for Ferroptosis of Macrophage after Spinal Cord Injury.Aging and disease · 2023Article
- Cathepsin B in programmed cell death machinery: mechanisms of execution and regulatory pathways.Cell death & disease · 2023Review
- Emerging roles of GPR109A in regulation of neuroinflammation in neurological diseases and pain.Neural regeneration research · 2023Review
- Ketogenic Diet Modulates Neuroinflammation via Metabolites from Lactobacillus reuteri After Repetitive Mild Traumatic Brain Injury in Adolescent Mice.Cellular and molecular neurobiology · 2023Article
- Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023Review
- Caspase-8 inactivation drives autophagy-dependent inflammasome activation in myeloid cells.Science advances · 2022Article
- Extralysosomal cathepsin B in central nervous system: Mechanisms and therapeutic implications.Brain pathology (Zurich, Switzerland) · 2022Review
- Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.Pharmacological reviews · 2022Review
- The Impact of Inflammatory Stimuli on Xylosyltransferase-I Regulation in Primary Human Dermal Fibroblasts.Biomedicines · 2022Article
- Role of cathepsin K in the expression of mechanical hypersensitivity following intra-plantar inflammation.Scientific reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-1β and IL-18 play critical roles in the induction of chronic pain hypersensitivity. Their inactive forms are activated by caspase-1. However, little is known about the mechanism underlying the activation of pro-caspase-1. There is increasing evidence that cathepsin B (CatB), a typical lysosomal cysteine protease, is involved in the pro-caspase-1 activation and the subsequent maturation of IL-1β and IL-18. In this context, CatB is considered to be an important molecular target to control chronic pain. However, no information is currently available about the role of CatB in chronic pain hypersensitivity. We herein show that CatB deficiency or the intrathecal administration of CA-074Me, a specific CatB inhibitor, significantly inhibited the induction of complete Freund's adjuvant-induced tactile allodynia in mice without affecting peripheral inflammation. In contrast, CatB deficiency did not affect the nerve injury-induced tactile allodynia. Furthermore, CatB deficiency or CA-074Me treatment significantly inhibited the maturation and secretion of IL-1β and IL-18 by cultured microglia following treatment with the neuroactive glycoprotein chromogranin A (CGA), but not with ATP. Moreover, the IL-1β expression in spinal microglia and the induction of tactile allodynia following the intrathecal administration of CGA depended on CatB, whereas those induced by the intrathecal administration of ATP or lysophosphatidic acid were CatB independent. These results strongly suggest that CatB is an essential enzyme for the induction of chronic inflammatory pain through its activation of pro-caspase-1, which subsequently induces the maturation and secretion of IL-1β and IL-18 by spinal microglia. Therefore, CatB-specific inhibitors may represent a useful new strategy for treating inflammation-associated pain.
Indexed as
Identifiers
What OpenQuestion holds
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.