Analysis of Common Pathways and Markers From Non-Alcoholic Fatty Liver Disease to Immune-Mediated Diseases.

dc.contributor.authorGallego-Duran, Rocio
dc.contributor.authorMontero-Vallejo, Rocio
dc.contributor.authorMaya-Miles, Douglas
dc.contributor.authorLucena, Ana
dc.contributor.authorMartin, Franz
dc.contributor.authorAmpuero, Javier
dc.contributor.authorRomero-Gomez, Manuel
dc.contributor.funderConsejería de Salud de la Junta de Andalucía
dc.contributor.funderMinisterio de Economía y Competitividad
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderFondo Europeo de Desarrollo Regional (FEDER)
dc.date.accessioned2025-01-07T17:25:52Z
dc.date.available2025-01-07T17:25:52Z
dc.date.issued2021-11-24
dc.description.abstractMetabolic associated fatty liver disease (MAFLD) is the most prevalent form of liver disease worldwide, accounting for a high liver-related mortality and morbidity with extensive multi-organ involvement. This entity has displaced viral hepatitis as the main cause of severe forms of hepatic diseases, although the onset and transition of MAFLD stages still remains unclear. Nevertheless, innate and adaptive immune responses seem to play an essential role in the establishment and further progression of this disease. The immune system is responsible of safeguard and preserves organs and systems function, and might be altered under different stimuli. Thus, the liver suffers from metabolic and immune changes leading to different injuries and loss of function. It has been stablished that cell-cell crosstalk is a key process in the hepatic homeostasis maintenance. There is mounting evidence suggesting that MAFLD pathogenesis is determined by a complex interaction of environmental, genetic and host factors that leads to a full plethora of outcomes. Therefore, herein we will revisit and discuss the interplay between immune mechanisms and MAFLD, highlighting the potential role of immunological markers in an attempt to clarify its relationship.
dc.description.versionSi
dc.identifier.citationGallego-Durán R, Montero-Vallejo R, Maya-Miles D, Lucena A, Martin F, Ampuero J, et al. Analysis of Common Pathways and Markers From Non-Alcoholic Fatty Liver Disease to Immune-Mediated Diseases. Front Immunol. 2021 Nov 24;12:667354.
dc.identifier.doi10.3389/fimmu.2021.667354
dc.identifier.essn1664-3224
dc.identifier.pmcPMC8652219
dc.identifier.pmid34899679
dc.identifier.pubmedURLhttps://pmc.ncbi.nlm.nih.gov/articles/PMC8652219/pdf
dc.identifier.unpaywallURLhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.667354/pdf
dc.identifier.urihttps://hdl.handle.net/10668/28371
dc.journal.titleFrontiers in immunology
dc.journal.titleabbreviationFront Immunol
dc.language.isoen
dc.organizationCentro Andaluz de Biología Molecular (CABIMER)
dc.organizationInstituto de Investigación Biomédica de Sevilla (IBIS)
dc.organizationSAS - Hospital Universitario Virgen del Rocío
dc.organizationSAS - Hospital Universitario Virgen del Rocío
dc.page.number11
dc.publisherFrontiers Research Foundation
dc.pubmedtypeJournal Article
dc.pubmedtypeResearch Support, Non-U.S. Gov't
dc.pubmedtypeReview
dc.relation.projectIDPC-0148-2016-0148
dc.relation.projectIDAGL2017-86927-R
dc.relation.projectIDPI16/01842
dc.relation.projectIDPI19/01404
dc.relation.projectIDPI19/00589
dc.relation.projectIDIFI18/00041
dc.relation.projectIDCD18/00126
dc.relation.projectIDPE-0451-2018
dc.relation.publisherversionhttps://doi.org/10.3389/fimmu.2021.667354
dc.rightsAttribution 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectNAFLD
dc.subjectNASH
dc.subjectbiomarkers
dc.subjectfibrosis
dc.subjectimmunology
dc.subject.decsEnfermedad
dc.subject.decsHígado
dc.subject.decsCélulas
dc.subject.decsContabilidad
dc.subject.decsSistema inmunológico
dc.subject.decsHígado graso
dc.subject.decsHeridas y lesiones
dc.subject.decsInmunidad
dc.subject.meshAnimals
dc.subject.meshHumans
dc.subject.meshNon-alcoholic Fatty Liver Disease
dc.titleAnalysis of Common Pathways and Markers From Non-Alcoholic Fatty Liver Disease to Immune-Mediated Diseases.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number12

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