ArticleMolecular medicine reports2017
JNK signaling is required for the MIP‑1α‑associated regulation of Kupffer cells in the heat stroke response.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Effects of Dominant Associated BacteriaMicroorganisms · 2025Article
- Heme oxygenase 1-mediated ferroptosis in Kupffer cells initiates liver injury during heat stroke.Acta pharmaceutica Sinica. B · 2024Article
- Article
- Multi-omics association study integrating GWAS and pQTL data revealed MIP-1α as a potential drug target for erectile dysfunction.Frontiers in pharmacology · 2024Article
- Physiological and Psychological Stress of Microwave Radiation-Induced Cardiac Injury in Rats.International journal of molecular sciences · 2023Article
- Alteration of gut microbiota after heat acclimation may reduce organ damage by regulating immune factors during heat stress.Frontiers in microbiology · 2023Article
- The pathogenesis and therapeutic strategies of heat stroke-induced liver injury.Critical care (London, England) · 2022Review
- Glycol-Chitosan-Based Technetium-99m-Loaded Multifunctional Nanomicelles: Synthesis, Evaluation, and In Vivo Biodistribution.Nanomaterials (Basel, Switzerland) · 2022Article
- Enhanced intestinal permeability and intestinal co-morbidities in heat strain: A review and case for autodigestion.Temperature (Austin, Tex.) · 2021Review
- Silencing of the MEKK2/MEKK3 Pathway Protects against Spinal Cord Injury via the Hedgehog Pathway and the JNK Pathway.Molecular therapy. Nucleic acids · 2019Article
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe heat stroke (HS) consists of extreme hyperthermia with thermoregulatory failure, leading to high morbidity and mortality. Liver injury is a complication of HS that is associated with inflammatory responses and Kupffer cells (KCs), which are resident macrophages in the liver that serve as a major source of inflammatory cytokines; however, the association and the underlying mechanisms of KC functions in HS‑induced endotoxemia and inflammation require an improved understanding. The important chemokine macrophage inflammatory protein‑1α (MIP‑1α) increases inflammatory responses and the secretion of inflammatory molecules from KCs, including tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6. In addition, the activation of c‑Jun N‑terminal kinase (JNK) signaling is responsible for the development of liver inflammation. Therefore, HS animal and cell models were constructed in order to investigate the pathways involved in the HS‑induced dysfunction of KCs. The results of the present study suggest that JNK may be involved in the MIP‑1α‑associated pathogenesis of KCs in HS injury.
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