ArticleMolecular medicine (Cambridge, Mass.)2025
HSPA1A inhibits pyroptosis and neuroinflammation after spinal cord injury via DUSP1 inhibition of the MAPK signaling pathway.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A three-gene signature correlated with MAPK/ERK activation characterizes acquired resistance to EGFR-tyrosine kinase inhibitors in non-small cell lung cancer.Oncology letters · 2026Article
- Captopril restores microglial homeostasis and reverses ASD-like phenotype in a model of ASD induced by exposure in utero to anti-caspr2 IgG.Molecular psychiatry · 2026Article
- Immune-dominated cellular heterogeneity and stromal plasticity in keloid infiltrating and hypercellular zones revealed by single-cell RNA sequencing.Frontiers in immunology · 2026Article
- Exploring the Potential Roles of Oxidative Stress-Related Genes in Thyroid Eye Disease and Graves' Disease.Journal of ophthalmology · 2026Article
- Limosilactobacillus reuteri DSM17938 Attenuates Neuroinflammatory Responses After Spinal Cord Injury by Modulating Tryptophan Metabolism.Probiotics and antimicrobial proteins · 2026Article
- Host stress proteins shape hemorrhagic shock via gut microbiota: evidence from Mendelian randomization and animal models.Journal of translational medicine · 2025Article
- Anti-inflammatory effects of natural polysaccharides: molecular mechanisms and nanotherapeutic applications.Frontiers in immunology · 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
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Authors and funding
11 authors.
Funding
Abstract
backgroundInflammation and proinflammatory programmed cell death, referred to as pyroptosis, are important causes of poor functional recovery after traumatic spinal cord injury (TSCI). Heat shock protein family A member 1A (HSPA1A) is a molecular chaperone protein that is highly expressed after TSCI and is thought to be neuroprotective. However, the mechanisms underlying the protective effects of HSPA1A after TSCI are unclear.
methodsThe levels of pyroptosis and inflammation after TSCI were determined by enzyme-linked immunosorbent assay (ELISA) and western blotting analysis. The role of HSPA1A in regulating pyroptosis and inflammation in TSCI was verified by in vivo and in vitro experiments. The molecular mechanism of the effects of HSPA1A in TSCI was elucidated by bioinformatics and coimmunoprecipitation analyses.
resultsPyroptosis and inflammation are significantly increased after TSCI. HSPA1A overexpression in microglia attenuated nigericin- and lipopolysaccharide (LPS)-induced pyroptosis and inflammation in vitro, whereas knockdown of HSPA1A aggravated pyroptosis and inflammation. In vivo, overexpression of HSPA1A reduced tissue damage, nerve cell death, pyroptosis, and inflammation in TSCI rats and promoted functional recovery. Mechanistically, we identified that HSPA1A interacts with dual specificity phosphatase 1 (DUSP1) and inhibits activation of the mitogen-activated protein kinase (MAPK) pathway, thereby attenuating pyroptosis and inflammation.
conclusionHSPA1A reduces pyroptosis and inflammation after TSCI by upregulating DUSP1 and inhibiting MAPK pathway activation. HSPA1A activation has potential as a therapeutic approach to promote functional recovery after TSCI.
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