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aocs, pubmed, immune, article, analysis, pathway, google, scholar, genes, cgassting, inflammatory, expression, cell, signaling, fig, cas, compartment, group, experimental, groups, enrichment, gene, syndrome, model, control, pathways, central, acute, cells, inflammation, slca, damage, disease, data, research, neutrophils, death, response, nfkbiz, activation, iron, upregulated, pressure, sequencing, mrna, role, rna, interaction, ptprc, forward,

Topics {✒️}

generation high-throughput sequencing account european journal ubiquitin-mediated protein hydrolysis acute compartment syndrome ischemia–reperfusion injury leads age-related macular degeneration regulating post-injury inflammation qrt-pcr reaction conditions cgas–sting pathway represents cgas–sting pathway components cgas–sting pathway modulators cgas-sting pathway controls renal ischemia/reperfusion injury medium-chain triglycerides decreases aging-related endothelial dysfunction european economic area cytokine–cytokine receptor interaction th2-type immune responses cgas–sting pathway plays mrna–mirna–lncrna integrated analysis nf-κb signaling pathway traditional central dogma protein-protein interaction networks cgas-sting inflammatory pathway privacy choices/manage cookies consequential ischemic damage skeletal muscle tissue immune-mediated inflammatory disease animals receive prompt iron-death-related genes mediating cellular uptake bmc cxcl1/cxcr2 axis enhances late-stage aocs patients neutrophil extracellular traps authors scientific editing guangxi medical university controlling nf-κb activity systemic iron homeostasis promotes disease progression nf-κb regulates ischemia-reperfusion injury neutrophil iron death cgas-sting signalling immune chemotaxis-related processes regulated cell death multi-omics sequencing minimizing animal suffering 2047-783x contact hepatocellular iron overload

Questions {❓}

• As an important mechanism for sensing abnormal intracellular DNA, the cGAS–STING pathway can enhance pathogen defense and regulate immune responses by activating the release of IFN?
• DAMPs, as critical factors in activating the cGAS–STING pathway [45], may regulate immune cell responses, including the production of IFN?
• In AOCS, tissue damage and DAMP release caused by ischemia may activate the cGAS–STING pathway, promote the production of IFN?
• Who is at risk?

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         description:Acute Osteofascial Compartment Syndrome (AOCS) stands as a critical surgical emergency, often secondary to various diseases. Its clinical manifestation arises from increased pressure within the fascial compartment, resulting in diminished tissue perfusion and consequential ischemic damage. Presently, clinical diagnostics lack effective biological markers, and patients face a grim prognosis, experiencing muscle contractures, necrosis, amputations, renal failure, and even mortality. The primary treatment, fasciotomy, poses infection risks and potential nerve damage. Hence, there is an urgent need for research elucidating AOCS's pathogenic mechanism and exploring novel treatments. To address this, we established a rat model of AOCS, extracting toe flexor muscles from both experimental and control groups. Employing second-generation high-throughput sequencing, we obtained comprehensive mRNA, lncRNA, circRNA, and miRNA data. Comparative analysis of expression differences between AOCS and control groups, followed by in-depth examination, allowed us to unravel the intricacies of AOCS occurrence from a multi-omics perspective. Our research findings indicate that AOCS is an immune-mediated inflammatory disease, primarily involving immune cells, especially neutrophils. In addition, genes associated with ferroptosis, a form of regulated cell death, are found to be upregulated in the rat model, with non-coding RNAs playing a role in regulatory interactions. These results suggest that neutrophils may undergo ferroptosis, thereby enhancing inflammation and immune responses in the fascial compartment, which promotes disease progression. Furthermore, these findings reveal the interactions between immune molecules and pathways in AOCS, which are significant for a deeper understanding of the pathogenesis of the disease and the development of targeted therapeutic strategies.
         datePublished:2025-02-05T00:00:00Z
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      headline:Immune-mediated mechanisms in acute osteofascial compartment syndrome: insights from multi-omics analysis
      description:Acute Osteofascial Compartment Syndrome (AOCS) stands as a critical surgical emergency, often secondary to various diseases. Its clinical manifestation arises from increased pressure within the fascial compartment, resulting in diminished tissue perfusion and consequential ischemic damage. Presently, clinical diagnostics lack effective biological markers, and patients face a grim prognosis, experiencing muscle contractures, necrosis, amputations, renal failure, and even mortality. The primary treatment, fasciotomy, poses infection risks and potential nerve damage. Hence, there is an urgent need for research elucidating AOCS's pathogenic mechanism and exploring novel treatments. To address this, we established a rat model of AOCS, extracting toe flexor muscles from both experimental and control groups. Employing second-generation high-throughput sequencing, we obtained comprehensive mRNA, lncRNA, circRNA, and miRNA data. Comparative analysis of expression differences between AOCS and control groups, followed by in-depth examination, allowed us to unravel the intricacies of AOCS occurrence from a multi-omics perspective. Our research findings indicate that AOCS is an immune-mediated inflammatory disease, primarily involving immune cells, especially neutrophils. In addition, genes associated with ferroptosis, a form of regulated cell death, are found to be upregulated in the rat model, with non-coding RNAs playing a role in regulatory interactions. These results suggest that neutrophils may undergo ferroptosis, thereby enhancing inflammation and immune responses in the fascial compartment, which promotes disease progression. Furthermore, these findings reveal the interactions between immune molecules and pathways in AOCS, which are significant for a deeper understanding of the pathogenesis of the disease and the development of targeted therapeutic strategies.
      datePublished:2025-02-05T00:00:00Z
      dateModified:2025-02-05T00:00:00Z
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         Ischemic damage
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         Ferroptosis
         CGAS–STING
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         Oncology
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      name:Department of Orthopedics Trauma and Hand Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China
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      name:Department of Orthopedics Trauma and Hand Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China

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