ArticleMolecular biotechnology2025
TRIM32 Inhibits NEK7 Ubiquitylation-Dependent Microglia Pyroptosis After Spinal Cord Injury.
Article in Molecular biotechnology, 2025. 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 5 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.
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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- TRIM32 drives head and neck squamous cell carcinoma progression via TP53 suppression and lysosomal/autophagy dysregulation.Translational cancer research · 2026Article
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025Review
- Microglial pyroptosis as a therapeutic target after traumatic spinal cord injury: current progress and future directions.Frontiers in immunology · 2025Review
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) is a disabling disease associated with microglial activation. Tripartite motif containing 32 (TRIM32) is an E3 ubiquitin ligase that plays a role in SCI. This study aimed to explore the role of TRIM32 in SCI and its potential mechanisms. We established an SCI mouse model to assess the function of TRIM32 using quantitative real-time polymerase chain reaction (qPCR), and hematoxylin and eosin staining. Additionally, a lipopolysaccharides (LPS)-induced cell injury model was generated to explore the impact of TRIM32 on pyroptosis using qPCR, propidium iodide staining, and western blotting. The ubiquitylation of NEK7 was analyzed using western blotting, co-immunoprecipitation, and immunofluorescence staining. The results showed that TRIM32 expression was increased in SCI mice and LPS-induced BV-2 cells. Overexpression of TRIM32 ameliorated SCI in mice and suppressed pyroptosis in LPS-treated BV-2 cells. Additionally, the E3 ligase TRIM32 promoted the ubiquitylation of NEK7 at the K64 site, leading to the downregulation of NEK7 levels. Inhibiting NEK7 ubiquitylation reversed the suppression of pyroptosis by TRIM32. In conclusion, TRIM32 inhibits microglia pyroptosis by facilitating the ubiquitylation of NEK7 at the K64 site, thereby alleviating the progression of SCI. The findings suggest that TRIM32 has the potential to be a therapeutic target of SCI.
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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.