ArticleFrontiers in immunology2021
Differential Regulation of Damage-Associated Molecular Pattern Release in a Mouse Model of Skeletal Muscle Ischemia/Reperfusion Injury.
Article in Frontiers in immunology, 2021. 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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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Barrier breakdown: lung-brain crosstalk in systemic inflammation.Journal of neuroinflammation · 2026Review
- HIF1A transcriptionally activates CDKN1A to drive ferroptosis in skeletal muscle ischaemia-reperfusion injury.Journal of orthopaedic translation · 2026Article
- Mouse Models of Muscle Fibrosis: Mechanisms, Methods, and Applications.Biomedicines · 2026Review
- Neutrophil Gelatinase-Associated Lipocalin: A Shared Early Biomarker of Remote Organ Dysfunction in Blast-Induced Extremity Trauma.International journal of molecular sciences · 2025Article
- Berbamine attenuates hind limb ischemia-reperfusion injury by eliminating lipid ROS and inhibiting p65 nuclear translocation.Frontiers in pharmacology · 2025Article
- Skeletal Muscle Damage and Inflammation.Advances in experimental medicine and biology · 2025Review
- ROS-scavenging ultrasonicated graphene oxide/alginate microgels for mesenchymal stem cell delivery and hindlimb ischemia treatment.Materials today. Bio · 2024Article
- Berbamine Promotes the Repair of Lower Limb Muscle Damage in Chronic Limb-Threatening Ischemia by Inhibiting Local Inflammation and NF-κB Nuclear Translocation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Emerging therapeutic strategies targeting extracellular histones for critical and inflammatory diseases: an updated narrative review.Frontiers in immunology · 2024Review
- Multiple site inflammation and acute kidney injury in crush syndrome.Frontiers in pharmacology · 2024Article
- Neutrophil extracellular traps and citrullinated fibrinogen contribute to injury in a porcine model of limb ischemia and reperfusion.Frontiers in immunology · 2024Article
- Delayed step-by-step decompression with DSF alleviates skeletal muscle crush injury by inhibiting NLRP3/CASP-1/GSDMD pathway.Cell death discovery · 2023Article
- Inflammation balance in skeletal muscle damage and repair.Frontiers in immunology · 2023Review
- Improving the ischemia-reperfusion injury in vascularized composite allotransplantation: Clinical experience and experimental implications.Frontiers in immunology · 2022Review
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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
Background: Skeletal muscle ischemia/reperfusion (I/R) injury is an important clinical issue that can cause remote organ injury. Although its pathogenesis has not been fully elucidated, recent studies have suggested that damage-associated molecular patterns (DAMPs) are mediators of remote organ injury in sterile inflammation. The purpose of this study was to investigate the possible involvement of DAMPs, including the nuclear proteins high-mobility group box 1 (HMGB1) and histone H3, in the pathogenesis of skeletal muscle I/R injury in mice. Methods: Hindlimb ischemia was induced in mice through bilateral ligation of inguinal regions using rubber grommets. Reperfusion was induced by cutting the rubber grommets after 2-12 h of ischemic period. Survival rates, localization of HMGB1 and histone H3 in the gastrocnemius muscle, and circulating HMGB1 and histone H3 levels were analyzed. The effect of anti-HMGB1 and anti-histone H3 antibodies on survival was analyzed in mice with I/R injury. Results: All mice with hindlimb ischemia survived for at least 36 h, while all mice died within 24 h if the hindlimbs were reperfused after ischemia for 4-12 h. Immunohistochemical analysis revealed that HMGB1 translocated from the nucleus to the cytoplasm in the ischemic gastrocnemius muscle, while histone H3 was confined to the nucleus. Accordingly, serum HMGB1 levels were significantly elevated in mice with hindlimb I/R compared with normal mice or mice with hindlimb ischemia ( Conclusions: HMGB1, but not histone H3, translocated to the cytoplasm during skeletal muscle ischemia, and was released into the systemic circulation after reperfusion in mice with I/R injury. Treatment with anti-HMGB1 antibodies partially improved survival.
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