ArticleJournal of orthopaedic surgery and research2017
Anti-high mobility group box-1 (HMGB1) antibody attenuates kidney damage following experimental crush injury and the possible role of the tumor necrosis factor-α and c-Jun N-terminal kinase pathway.
Article in Journal of orthopaedic surgery and research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 30 citations in OpenAlex.
- Inhibition of eCIRP Attenuates Inflammation and Gut Injury After Radiation Combined Injury with Sepsis.Medical sciences (Basel, Switzerland) · 2026Article
- Risk factors associated with postoperative necrosis after digital replantation: a systematic review and meta-analysis.Frontiers in surgery · 2026Review
- Crush injury and crush syndrome: a comprehensive review.EFORT open reviews · 2025Article
- Rescue RM/CS-AKI by blocking strategy with one-dose anti-myoglobin RabMAb.Nature communications · 2025Article
- Advancing crush syndrome management: the potent role of Sodium zirconium cyclosilicate in early hyperkalemia intervention and survival enhancement in a rat model.Frontiers in pharmacology · 2024Article
- DAMPs and radiation injury.Frontiers in immunology · 2024Review
- Clinical diagnoses associated with a positive antinuclear antibody test in patients with and without autoimmune disease.BMC rheumatology · 2023Article
- Zinc chelator treatment in crush syndrome model mice attenuates ischemia-reperfusion-induced muscle injury due to suppressing of neutrophil infiltration.Scientific reports · 2022Article
- β1-Blocker improves survival and ventricular remodelling in rats with lethal crush injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries.Journal of orthopaedic surgery and research · 2022Article
- Anti-high mobility group box protein 1 monoclonal antibody downregulating P-glycoprotein as novel epilepsy therapeutics.The Egyptian journal of neurology, psychiatry and neurosurgery · 2022Review
- RIG-I, a novel DAMPs sensor for myoglobin activates NF-κB/caspase-3 signaling in CS-AKI model.Military Medical Research · 2021Article
- Emerging medical therapies in crush syndrome - progress report from basic sciences and potential future avenues.Renal failure · 2020Review
- Damage-associated molecular patterns in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2020Review
- Danger signals in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation plays a crucial role in kidney damage after crush syndrome (CS). Several researchers report that high mobility group box-1 protein (HMGB1) may be the vital trigger in kidney damage, and tumor necrosis factor-α (TNF-α) and c-Jun N-terminal kinase (JNK) are involve in this pathophysiological process, but their biological roles are unclear. This study aimed to explore the relationship between HMGB1, JNK, and TNF-α in kidney damage.
methodsThe crush injury model was established using weight compression. The reliability of the crush injury model was determined by hematoxylin-eosin (HE) staining. Western blot was used to detect the expression of HMGB1, JNK, and TNF-α, and TUNEL was used to mark apoptotic cells in the renal cortex.
resultsThe results showed that the highest expression of HMGB1 in muscle was 12 h after CS. JNK and TNF-α increased and peaked at 1 day after CS in kidneys. Western blot analysis revealed that anti-HMGB1 antibody could downregulate the expression of JNK and TNF-α. Anti-TNF-α could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-α in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-α antibody, and SP600125 could reduce cellular apoptosis in the renal cortex.
conclusionsIt is possible that JNK and TNF-α commonly contribute to kidney damage by assembling a positive feedback cycle after CS, leading to increased apoptosis in the renal cortex. HMGB1 from the muscle may be the trigger.
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