ArticleJournal of inflammation research2022
UCHL1 Promoted Polarization of M1 Macrophages by Regulating the PI3K/AKT Signaling Pathway.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 22 citations in OpenAlex.
- Engineered thoracic spinal cord organoids for transplantation after spinal cord injury.Nature biomedical engineering · 2026Article
- UCHL1 Promotes M1 Macrophage Polarization and Inflammation in Chronic Rhinosinusitis by Stabilizing HIF-1α.Cell biochemistry and biophysics · 2026Article
- The Emerging Role of UCHL1 in Neurological and Musculoskeletal Diseases.Immunology and cell biology · 2026Review
- Prevotella copri promotes white adipose browning and ameliorates adiposity.Nature communications · 2025Article
- Ubiquitin C-terminal hydrolase L1 promoted pro-angiogenic capacity of periodontal ligament stem cells via HIF-1α/YAP signaling in periodontitis.Stem cell research & therapy · 2025Article
- LMTK3 regulation of EV biogenesis and cargo sorting promotes tumour growth by reducing monocyte infiltration and driving pro-tumourigenic macrophage polarisation in breast cancer.Molecular cancer · 2025Article
- Elevated Cerebrospinal Fluid Ubiquitin Carboxyl-Terminal Hydrolase Isozyme L1 in Asymptomatic C9orf72 Hexanucleotide Repeat Expansion Carriers.Annals of neurology · 2025Observational
- Signaling Pathways Involved in Acute Pancreatitis.Journal of inflammation research · 2025Review
- Ubiquitination in macrophage plasticity: from inflammatory to immunometabolic pathways.Frontiers in immunology · 2025Review
- Decoding the hypoxia-exosome-immune triad in OSA: PRCP/UCHL1/BTG2-driven metabolic dysregulation revealed by interpretable machine learning.Frontiers in immunology · 2025Article
- Predicting immunotherapy efficacy in endometrial cancer: focus on the tumor microenvironment.Frontiers in immunology · 2024Review
- USP12 promotes antiviral responses by deubiquitinating and stabilizing IFI16.PLoS pathogens · 2023Article
- USP1-regulated reciprocal differentiation of Th17 cells and Treg cells by deubiquitinating and stabilizing TAZ.Cellular & molecular immunology · 2023Article
- TRIM21 aggravates cardiac injury after myocardial infarction by promoting M1 macrophage polarization.Frontiers in immunology · 2022Article
- Time Series Transcriptomic Analysis by RNA Sequencing Reveals a Key Role of PI3K in Sepsis-Induced Myocardial Injury in Mice.Frontiers in physiology · 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
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs deubiquitinases (DUBs), ubiquitin C-terminal hydrolase (UCH)-L1 has been shown to play a crucial role in regulating diverse biological processes. However, its function in macrophage polarization remains unclear.
methodsWe performed in vivo and in vitro experiments to investigate the role of ubiquitin carboxyl-terminal hydrolase L1 (UCHL1), a kind of DUBs, in macrophage differentiation by using UCHL1-deficiency mice.
resultsWe demonstrated that LPS stimulation induced UCHL1 expression in macrophages. The deficiency of UCHL1 expression decreased the expression of CD80 and CD86 but increased the expression of CD206. The expression of TNF-α, IL-6, iNOS, and IL-10 was downregulated, while that of Arg1, Ym1, and Fizz1 was upregulated in UCHL1 deficient macrophages. Moreover, we observed that UCHL1 promoted the degradation of p110α through autophagy, but paradoxically increased the activity of AKT, thereby promoting polarization of macrophages into pro-inflammatory states.
conclusionIn this study, we identified UCHL1 as a positive regulator of M1 macrophage polarization. Our findings may help in developing therapeutic interventions for the treatment of inflammatory diseases and pathogenic infections.
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.