ArticleMolecular medicine (Cambridge, Mass.)
Caspase-1 is hepatoprotective during trauma and hemorrhagic shock by reducing liver injury and inflammation.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- Caspase-11 regulates systemic inflammation and cell death in a cell-specific manner after trauma with shock.Journal of leukocyte biology · 2025Article
- Exploring caspase functions in mouse models.Apoptosis : an international journal on programmed cell death · 2024Review
- NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases-A Lesson from Cytokine Storm Syndrome.International journal of molecular sciences · 2023Review
- Hepatocyte-specific regulation of autophagy and inflammasome activation via MyD88 during lethalFrontiers in immunology · 2023Article
- Review: Protective Immunity and Immunopathology of Ehrlichiosis.Zoonoses (Shannon, Ireland) · 2022Article
- Pyroptosis in sepsis: Comprehensive analysis of research hotspots and core genes in 2022.Frontiers in molecular biosciences · 2022Article
- Gasdermin D protects against noninfectious liver injury by regulating apoptosis and necroptosis.Cell death & disease · 2019Article
- Old Friends, immunoregulation, and stress resilience.Pflugers Archiv : European journal of physiology · 2019Review
- Remifentanil upregulates hepatic IL-18 binding protein (IL-18BP) expression through transcriptional control.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Anti-inflammatory effect of Resolvin D1 on LPS-treated MG-63 cells.Experimental and therapeutic medicine · 2018Article
- Regulation of epithelial injury and bile duct obstruction by NLRP3, IL-1R1 in experimental biliary atresia.Journal of hepatology · 2018Article
- Macrophages play an essential role in trauma-induced sterile inflammation and tissue repair.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018Review
- Observational
- Inflammasome: A Double-Edged Sword in Liver Diseases.Frontiers in immunology · 2018Review
- Inhibition of BTK protects lungs from trauma-hemorrhagic shock-induced injury in rats.Molecular medicine reports · 2017Article
- NK1.1Journal of leukocyte biology · 2017Article
- Progresses in understanding trauma-induced coagulopathy and the underlying mechanism.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2017Review
- Redox-dependent regulation of hepatocyte absent in melanoma 2 inflammasome activation in sterile liver injury in mice.Hepatology (Baltimore, Md.) · 2017Article
- Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.Transplantation · 2016Review
- Caspase-1 Activation Protects Lung Endothelial Barrier Function during Infection-Induced Stress.American journal of respiratory cell and molecular biology · 2016Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Adaptive immune responses are induced in liver after major stresses such as hemorrhagic shock (HS) and trauma. There is emerging evidence that the inflammasome, the multiprotein platform that induces caspase-1 activation and promotes interleukin (IL)-1β and IL-18 processing, is activated in response to cellular oxidative stress, such as after hypoxia, ischemia and HS. Additionally, damage-associated molecular patterns, such as those released after injury, have been shown to activate the inflammasome and caspase-1 through the NOD-like receptor (NLR) NLRP3. However, the role of the inflammasome in organ injury after HS and trauma is unknown. We therefore investigated inflammatory responses and end-organ injury in wild-type (WT) and caspase-1(-/-)mice in our model of HS with bilateral femur fracture (HS/BFF). We found that caspase-1(-/-) mice had higher levels of systemic inflammatory cytokines than WT mice. This result corresponded to higher levels of liver damage, cell death and neutrophil influx in caspase-1(-/-) liver compared with WT, although there was no difference in lung damage between experimental groups. To determine if hepatoprotection also depended on NLRP3, we subjected NLRP3(-/-) mice to HS/BFF, but found inflammatory responses and liver damage in these mice was similar to WT. Hepatoprotection was also not due to caspase-1-dependent cytokines, IL-1β and IL-18. Altogether, these data suggest that caspase-1 is hepatoprotective, in part through regulation of cell death pathways in the liver after major trauma, and that caspase-1 activation after HS/BFF does not depend on NLRP3. These findings may have implications for the treatment of trauma patients and may lead to progress in prevention or treatment of multiple organ failure (MOF).
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