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Insights into Macrophage/Monocyte-Endothelial Cell Crosstalk in the Liver

2021-03-17Recensão Acesso aberto
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dc.contributor.authorCoelho, Inês
dc.contributor.authorDuarte, Nádia
dc.contributor.authorMacedo, Maria Paula
dc.contributor.authorPenha-Gonçalves, Carlos
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2021-04-22T22:47:09Z
dc.date.available2021-04-22T22:47:09Z
dc.date.issued2021-03-17
dc.descriptionFunding: This work was funded with the support of Ferring innovation grant 2019 from Ferring Research Institute, Gilead Genese 2019 from Gilead Sciences Lda, “Fundação para a Ciência e Tecnologia” (PTDC/MEC447 MET/29314/2017) and iNOVA4Health (UIDB/Multi/04462/2020).
dc.description.abstractLiver disease accounts for millions of deaths worldwide annually being a major cause of global morbidity. Hepatotoxic insults elicit a multilayered response involving tissue damage, inflammation, scar formation, and tissue regeneration. Liver cell populations act coordinately to maintain tissue homeostasis and providing a barrier to external aggressors. However, upon hepatic damage, this tight regulation is disrupted, leading to liver pathology which spans from simple steatosis to cirrhosis. Inflammation is a hallmark of liver pathology, where macrophages and endothelial cells are pivotal players in promoting and sustaining disease progression. Understanding the drivers and mediators of these interactions will provide valuable information on what may contribute to liver resilience against disease. Here, we summarize the current knowledge on the role of macrophages and liver sinusoidal endothelial cells (LSEC) in homeostasis and liver pathology. Moreover, we discuss the expanding body of evidence on cell-to-cell communication between these two cell compartments and present triggering receptor expressed on myeloid cells-2 (Trem-2) as a plausible mediator of this cellular interlink. This review consolidates relevant knowledge that might be useful to guide the pursue of successful therapeutic targets and pharmacological strategies for controlling liver pathogenesis.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1302524
dc.identifier.doi10.3390/jcm10061248
dc.identifier.issn2077-0383
dc.identifier.otherPURE: 29221209
dc.identifier.otherPURE UUID: 92a6bb2c-cc89-4941-8f35-7b226ea7c3f0
dc.identifier.otherPubMed: 33802948
dc.identifier.otherPubMedCentral: PMC8002813
dc.identifier.otherWOS: 000651959300001
dc.identifier.otherScopus: 85114066772
dc.identifier.urihttp://hdl.handle.net/10362/116014
dc.language.isoeng
dc.peerreviewedyes
dc.subjectmacrophages
dc.subjectendothelial cells
dc.subjectliver disease
dc.subjectcell interactions
dc.subjectTrem-2
dc.titleInsights into Macrophage/Monocyte-Endothelial Cell Crosstalk in the Liveren
dc.title.subtitleA Role for Trem-2en
dc.typereview
degois.publication.issue6
degois.publication.titleJournal of Clinical Medicine
degois.publication.volume10
dspace.entity.typePublication
rcaap.rightsopenAccess

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