FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4385337704> ?p ?o ?g. }

• W4385337704 endingPage "887" @default.
• W4385337704 startingPage "885" @default.
• W4385337704 abstract "Neutrophils are the most abundant leukocytes in human peripheral blood; as part of the innate immune system, they are traditionally attributed a key role in acute inflammation as well as in host defense. For a long time, neutrophils were solely looked upon as a uniform mass of first responders in the clearance of invading pathogens. However, in contrast to these preconceptions, there is growing evidence of the importance of neutrophils in chronic inflammation, including in atherosclerosis, neurodegeneration and inflammatory bowel disease [1] Soehnlein O. Steffens S. Hidalgo A. Weber C. Neutrophils as protagonists and targets in chronic inflammation. Nat Rev Immunol. 2017; 17: 248-261https://doi.org/10.1038/nri.2017.10 Crossref PubMed Scopus (320) Google Scholar , as well as of their heterogeneity [2] Silvestre-Roig C. Hidalgo A. Soehnlein O. Neutrophil heterogeneity: implications for homeostasis and pathogenesis. Blood. 2016; 127: 2173-2181https://doi.org/10.1182/blood-2016-01-688887 Crossref PubMed Scopus (280) Google Scholar . While various subsets in physiological as well as pathological settings have been characterized in recent years [2] Silvestre-Roig C. Hidalgo A. Soehnlein O. Neutrophil heterogeneity: implications for homeostasis and pathogenesis. Blood. 2016; 127: 2173-2181https://doi.org/10.1182/blood-2016-01-688887 Crossref PubMed Scopus (280) Google Scholar ,[3] Xie X. Shi Q. Wu P. Zhang X. Kambara H. Su J. et al. Single-cell transcriptome profiling reveals neutrophil heterogeneity in homeostasis and infection. Nat Immunol. 2020; 21: 1119-1133https://doi.org/10.1038/s41590-020-0736-z Crossref PubMed Scopus (214) Google Scholar , it is a striking feature of neutrophils that this cell – originally thought to be terminally differentiated when exiting the bone marrow – can adopt a tissue-specific phenotype similar to what has previously been shown for macrophages [4] Ballesteros I. Rubio-Ponce A. Genua M. Lusito E. Kwok I. Fernández-Calvo G. et al. Co-option of Neutrophil Fates by Tissue Environments. Cell. 2020; 183: 1282-1297.e18https://doi.org/10.1016/j.cell.2020.10.003 Abstract Full Text Full Text PDF PubMed Scopus (166) Google Scholar ,[5] Lavin Y. Winter D. Blecher-Gonen R. David E. Keren-Shaul H. Merad M. et al. Tissue-resident macrophage enhancer landscapes are shaped by the local microenvironment. Cell. 2014; 159: 1312-1326https://doi.org/10.1016/j.cell.2014.11.018 Abstract Full Text Full Text PDF PubMed Scopus (1392) Google Scholar . Although neutrophil infiltration is a common feature in almost all settings of liver injury, their role, especially in chronic liver disease, has only lately come into focus. In this issue of the Journal of Hepatology, a study by Ariño and colleagues proofs the importance of neutrophil activity in chronic liver injury and reveals possible means of therapeutic interference in a disease setting where up to now treatment options were still relatively scarce. Specifically, the authors show that neutrophils are attracted to the periportal area in a chronic liver injury model; there, they adopt a distinguishable phenotype and perpetuate hepatic injury, while inhibition of neutrophil effector functions ameliorates tissue damage [6] Ariño S. Aguilar-Bravo B. Coll M. Lee W.-Y. Peiseler M. Paula Cantallops-Vilà nullDuctular reaction-associated neutrophils promote biliary epithelium proliferation in chronic liver disease. J Hepatol. 2023; (00423-3): S0168-8278https://doi.org/10.1016/j.jhep.2023.05.045 Abstract Full Text Full Text PDF Google Scholar . Ductular reaction-associated neutrophils promote biliary epithelium proliferation in chronic liver diseaseJournal of HepatologyPreviewDuctular reaction expansion is associated with poor prognosis in patients with advanced liver disease. However, the mechanisms promoting biliary cell proliferation are largely unknown. Here, we identify neutrophils as drivers of biliary cell proliferation and the defective wound-healing response. Full-Text PDF" @default.
• W4385337704 created "2023-07-29" @default.
• W4385337704 creator A5017294918 @default.
• W4385337704 creator A5027343879 @default.
• W4385337704 date "2023-10-01" @default.
• W4385337704 modified "2023-09-23" @default.
• W4385337704 title "DRANquilizing neutrophil function in chronic liver disease" @default.
• W4385337704 cites W2019676650 @default.
• W4385337704 cites W2087481743 @default.
• W4385337704 cites W2100186921 @default.
• W4385337704 cites W2112671019 @default.
• W4385337704 cites W2126811287 @default.
• W4385337704 cites W2135031001 @default.
• W4385337704 cites W2199531933 @default.
• W4385337704 cites W2317865868 @default.
• W4385337704 cites W2596984373 @default.
• W4385337704 cites W2902618639 @default.
• W4385337704 cites W2904922651 @default.
• W4385337704 cites W2920290417 @default.
• W4385337704 cites W2921439670 @default.
• W4385337704 cites W2958258302 @default.
• W4385337704 cites W3002371404 @default.
• W4385337704 cites W3044190151 @default.
• W4385337704 cites W3093916434 @default.
• W4385337704 cites W3163123861 @default.
• W4385337704 cites W4293182206 @default.
• W4385337704 cites W4381333059 @default.
• W4385337704 doi "https://doi.org/10.1016/j.jhep.2023.07.019" @default.
• W4385337704 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37517456" @default.
• W4385337704 hasPublicationYear "2023" @default.
• W4385337704 type Work @default.
• W4385337704 citedByCount "0" @default.
• W4385337704 crossrefType "journal-article" @default.
• W4385337704 hasAuthorship W4385337704A5017294918 @default.
• W4385337704 hasAuthorship W4385337704A5027343879 @default.
• W4385337704 hasConcept C126322002 @default.
• W4385337704 hasConcept C136449434 @default.
• W4385337704 hasConcept C203014093 @default.
• W4385337704 hasConcept C2776914184 @default.
• W4385337704 hasConcept C2779473830 @default.
• W4385337704 hasConcept C2780942790 @default.
• W4385337704 hasConcept C55493867 @default.
• W4385337704 hasConcept C63645605 @default.
• W4385337704 hasConcept C71924100 @default.
• W4385337704 hasConcept C83867959 @default.
• W4385337704 hasConcept C86803240 @default.
• W4385337704 hasConcept C8891405 @default.
• W4385337704 hasConceptScore W4385337704C126322002 @default.
• W4385337704 hasConceptScore W4385337704C136449434 @default.
• W4385337704 hasConceptScore W4385337704C203014093 @default.
• W4385337704 hasConceptScore W4385337704C2776914184 @default.
• W4385337704 hasConceptScore W4385337704C2779473830 @default.
• W4385337704 hasConceptScore W4385337704C2780942790 @default.
• W4385337704 hasConceptScore W4385337704C55493867 @default.
• W4385337704 hasConceptScore W4385337704C63645605 @default.
• W4385337704 hasConceptScore W4385337704C71924100 @default.
• W4385337704 hasConceptScore W4385337704C83867959 @default.
• W4385337704 hasConceptScore W4385337704C86803240 @default.
• W4385337704 hasConceptScore W4385337704C8891405 @default.
• W4385337704 hasIssue "4" @default.
• W4385337704 hasLocation W43853377041 @default.
• W4385337704 hasLocation W43853377042 @default.
• W4385337704 hasOpenAccess W4385337704 @default.
• W4385337704 hasPrimaryLocation W43853377041 @default.
• W4385337704 hasRelatedWork W1175477002 @default.
• W4385337704 hasRelatedWork W1987712008 @default.
• W4385337704 hasRelatedWork W2016026239 @default.
• W4385337704 hasRelatedWork W2141330728 @default.
• W4385337704 hasRelatedWork W2186316345 @default.
• W4385337704 hasRelatedWork W2357642782 @default.
• W4385337704 hasRelatedWork W2476770332 @default.
• W4385337704 hasRelatedWork W2792679014 @default.
• W4385337704 hasRelatedWork W3027247668 @default.
• W4385337704 hasRelatedWork W4281729072 @default.
• W4385337704 hasVolume "79" @default.
• W4385337704 isParatext "false" @default.
• W4385337704 isRetracted "false" @default.
• W4385337704 workType "article" @default.