ArticleJournal of immunology research2021
Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1.
Article in Journal of immunology research, 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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15 citing papers in PubMed, 28 citations in OpenAlex.
- Exploring the Molecular Mechanisms of Autophagy-related Genes in Hepatic Ischemia/Reperfusion Injury Using Bioinformatics.Transplantation direct · 2025Article
- Mechanism of action of the nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome and its regulation in liver injury.Chinese medical journal · 2025Review
- SYK promotes the formation of neutrophil extracellular traps by inducing PKM2 nuclear translocation and promoting STAT3 phosphorylation to exacerbate hepatic ischemia-reperfusion injury and tumor recurrence.Molecular medicine (Cambridge, Mass.) · 2024Article
- Specific knockout of notch-1 attenuates non-alcoholic fatty liver disease by promoting SHP2 phosphorylation.Aging · 2023Article
- Autophagy in hepatic ischemia-reperfusion injury.Cell death discovery · 2023Review
- Hepatocyte SGK1 activated by hepatic ischemia-reperfusion promotes the recurrence of liver metastasis via IL-6/STAT3.Journal of translational medicine · 2023Article
- Transcriptomics Analysis Revealed Key Genes Associated with Macrophage Autophagolysosome in Male ApoEJournal of inflammation research · 2023Article
- Vitamin D receptor mediates liver ischemia and reperfusion injury by autophagy-regulated M2 macrophage polarization.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Emerging Role of NLRP3 Inflammasome and Pyroptosis in Liver Transplantation.International journal of molecular sciences · 2022Review
- The multifunctional roles of autophagy in the innate immune response: Implications for regulation of transplantation rejection.Frontiers in cell and developmental biology · 2022Review
- The Role of NLRP3 Inflammasome Activation Pathway of Hepatic Macrophages in Liver Ischemia-Reperfusion Injury.Frontiers in immunology · 2022Review
- NLRP3: Role in ischemia/reperfusion injuries.Frontiers in immunology · 2022Review
- Article
- Targeting SYK of monocyte-derived macrophages regulates liver fibrosis via crosstalking with Erk/Hif1α and remodeling liver inflammatory environment.Cell death & disease · 2021Article
- The Interplay between Autophagy and NLRP3 Inflammasome in Ischemia/Reperfusion Injury.International journal of molecular sciences · 2021Review
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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
At present, liver ischemia-reperfusion (IR) injury is still a great challenge for clinical liver partial resection and liver transplantation. The innate immunity regulated by liver macrophages orchestrates the cascade of IR inflammation and acts as a bridge. As a specific macrophage subunit of vacuolar ATPase, ATP6V0D2 (V-ATPase D2 subunit) has been shown to promote the formation of autophagolysosome in vitro. Our research fills a gap which has existed in the study of inflammatory stress about the V-ATPase subunit ATP6V0D2 in liver macrophages. We first found that the expression of specific ATP6V0D2 in liver macrophages was upregulated with the induction of inflammatory cascade after liver IR surgery, and knockdown of ATP6V0D2 resulted in increased secretion of proinflammatory factors and chemokines, which enhanced activation of NLRP3 and aggravation of liver injury. Further studies found that the exacerbated activation of NLRP3 was related to the autophagic flux regulated by ATP6V0D2. Knocking down ATP6V0D2 impaired the formation of autophagolysosome and aggravated liver IR injury through nonspecific V-ATPase activation independent of V-ATPase-Notchl-Hesl signal axis. In general, we illustrated that the expression of ATP6V0D2 in liver macrophages was upregulated after liver IR, and by gradually promoting the formation of autophagolysosomes to increase autophagy flux to limit the activation of liver inflammation, this regulation is independent of the Notch1-Hes1 signal axis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.