ArticleFrontiers in cell and developmental biology2021
The Lipopolysaccharide-Sensing Caspase(s)-4/11 Are Activated in Cirrhosis and Are Causally Associated With Progression to Multi-Organ Injury.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Microplastics, nanoplastics and liver disease: an emerging health concern?Nature reviews. Gastroenterology & hepatology · 2026Review
- A new paradigm: 46 structural cell types function as environment-supporting innate immune cells, with endothelial and vascular smooth muscle cells as key prototypes.iNew medicine · 2026Article
- Interaction of inflammation and portal hypertension in cirrhosis progression.Nature reviews. Gastroenterology & hepatology · 2025Review
- Novel Therapeutic Approaches in Treatment of Acute-on-Chronic Liver Failure.Seminars in liver disease · 2023Review
- Vaccination in liver diseases and liver Transplantation: Recommendations, implications and opportunities in the post-covid era.JHEP reports : innovation in hepatology · 2023Review
- Role and significance of SIRT1 in regulating the LPS-activated pyroptosis pathway in children with congenital hydronephrosis.World journal of pediatric surgery · 2023Article
- SARS-CoV-2 infection and liver involvement.Hepatology international · 2022Review
- A novel pyroptosis-related gene signature for predicting laryngeal carcinoma prognosis.International journal of clinical and experimental pathology · 2022Article
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Authors and funding
19 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsThe development of multi-organ injury in cirrhosis is associated with increased intestinal permeability, translocation of gut-derived bacterial products [e.g., lipopolysaccharide (LPS)] into the circulation, and increased non-apoptotic hepatocyte cell death. Pyroptosis is a non-apoptotic, lytic form of cell death mediated by the LPS-sensing caspase(s)-4/11 (caspase-4 in humans, caspase-11 in mice), which leads to activation of the effector protein Gasdermin D (GSDMD) and subsequent formation of pores in the plasma membrane. Endoplasmic reticulum (ER) stress, a feature of cirrhosis, has been identified as a factor promoting the activation of caspase-11, thus increasing sensitivity of the cell to LPS-mediated pyroptosis. The aim of this study was to determine the role of bacterial LPS in the activation of hepatic caspase(s)-4/11 and progression of hepatic and extra-hepatic organ injury in cirrhosis. MATERIALS AND
methodsHuman liver samples from patients with stable cirrhosis (SC) or acutely decompensated cirrhosis (AD) were analyzed for caspase-4 activation by immunohistochemistry. Wild-type and
resultsHuman liver samples demonstrated increased caspase-4 activation in AD cirrhosis. Caspase-4 activation was associated with MELD score and circulating levels of LDH. Wild-type mice treated with CCl
conclusionThese data demonstrate for the first time a causal relationship between LPS-mediated activation of caspase(s)-4/11 and development of hepatic and extra-hepatic injury in cirrhosis.
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