ArticleMedComm2022
NOD1 induces pyroptotic cell death to aggravate liver ischemia-reperfusion injury in mice.
Article in MedComm, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Cell death in ischemia-reperfusion injury: beyond a single-cell-death perspective.Biomarker research · 2026Review
- Construction of Curcumin-Loaded Mesenchymal Stem Cell-Derived Exosomes and Their Mechanism in Inhibiting Pyroptosis During Hepatic Ischemia-Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Sterile Inflammation and Cell Death Pathways in Liver Ischemia-Reperfusion Injury: A Review and Perspective.Endocrine, metabolic & immune disorders drug targets · 2026Review
- Natural killer cell-derived granzyme B as a therapeutic target for alleviating graft injury during liver transplantation.Acta pharmaceutica Sinica. B · 2025Article
- S-nitrosylated NEDD4 exacerbates gouty arthritis by upregulating NOD1 to induce pyroptosis.Genes and immunity · 2025Article
- Programmed cell death, from liver Ischemia-Reperfusion injury perspective: An overview.Heliyon · 2024Review
- Cell Death in Liver Disease and Liver Surgery.Biomedicines · 2024Review
- Gp78 deficiency in hepatocytes alleviates hepatic ischemia-reperfusion injury via suppressing ACSL4-mediated ferroptosis.Cell death & disease · 2023Article
- Role of the immune system in liver transplantation and its implications for therapeutic interventions.MedComm · 2023Review
- NOD1 induces pyroptotic cell death to aggravate liver ischemia-reperfusion injury in mice.MedComm · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-binding oligomerization domain 1 (NOD1) can direct the release of inflammatory factors and influence autophagy and apoptosis in hepatic ischemia-reperfusion injury (IRI) in mice. As pyroptosis is involved in a number of inflammatory reactions, in this report, we investigated the potential for NOD1 to affect pyroptosis. We found that an increased expression of NOD1 during IRI was related to activation of the pyroptotic signaling pathway. With NOD1 activation, cleavage fragments of Caspase-1, gasdermin D (GSDMD), and interleukin (IL)-1β were all increased. Moreover, downregulation of NOD1 expression in AML12 cells exerted an opposite effect. Expression levels of cleaved-Caspase-1 and cleaved-GSDMD decreased after exposure to IRI and the number of cell membrane pores and apoptotic or pyroptotic cells decreased, along with the contents of inflammatory factors and lactate dehydrogenase in the supernatants of AML12 cells. Based on these findings, we conclude that NOD1 aggravates the pyroptotic cell death associated with hepatic ischemia-reperfusion injury in a mouse model via the Caspase-1/GSDMD axis. These findings help to alleviate pyroptotic cell death during liver transplantation or resection, providing new insights into novel protective therapies for liver IRI.
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