ArticleInflammation2020
HIPK3 Mediates Inflammatory Cytokines and Oxidative Stress Markers in Monocytes in a Rat Model of Sepsis Through the JNK/c-Jun Signaling Pathway.
Article in Inflammation, 2020. 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, 15 citations in OpenAlex.
- SNORC knockdown alleviates inflammation, autophagy defect and matrix degradation of chondrocytes in osteoarthritis development.Molecular and cellular biochemistry · 2024Article
- Microglia-derived CXCL2 induced neuronal ferroptosis via CXCR2/Jun axis in sepsis-associated encephalopathy.Frontiers in immunology · 2024Article
- Pharmacological effects and the related mechanism of scutellarin on inflammation-related diseases: a review.Frontiers in pharmacology · 2024Review
- Utilize proteomic analysis to identify potential therapeutic targets for combating sepsis and sepsis-related death.Frontiers in endocrinology · 2024Article
- Nerve Growth Factor and Autoimmune Diseases.Current issues in molecular biology · 2023Review
- Article
- Transcriptomic and proteomic profiling of the anterior cingulate cortex in neuropathic pain model rats.Frontiers in molecular neuroscience · 2023Article
- Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis.Cell death & disease · 2022Article
- MiR-146a upregulates FOXP3 and suppresses inflammation by targeting HIPK3/STAT3 in allergic conjunctivitis.Annals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a fetal immunological disorder and its complication worsens in the patients with hemodialysis which may increase the risk of death. In the present study, we aimed to investigate the effect of homeodomain-interacting protein kinase 3 (HIPK3) on inflammatory factors and oxidative stress markers in monocytes of rats with sepsis by regulating the c-Jun amino-terminal kinase (JNK)/c-Jun signaling pathway. A rat model of sepsis was initially established using cecal ligation and puncture (CLP) and was further identified by enlarged spleen tissues, inflammation, and oxidative stress. Monocytes were isolated from rats with CLP-induced sepsis. HIPK3 was observed to be downregulated while JUN was upregulated in monocytes from rats with CLP-induced sepsis. Furthermore, isolated monocytes were transduced with lentiviral vectors expressing HIPK3 or shRNA against HIPK3 to explore the effect of HIPK3 on viability and apoptosis of monocytes as well as inflammatory factors and oxidative stress markers. The obtained data exhibited that overexpression of HIPK3 or inhibition of the JNK signaling pathway enhanced proliferation, reduced apoptosis of monocytes, alleviated inflammation, and oxidative stress injury. Consistently, our results may provide evidence that HIPK3 could inhibit the JNK/c-Jun signaling pathway, thereby potentially retarding the progression of sepsis.
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