title: The Role of Tissue Macrophage-Mediated Inflammation on NAFLD Pathogenesis and Its Clinical Implications.
abstract: The obese phenotype is characterized by a state of chronic low-grade systemic inflammation that contributes to the development of comorbidities, including nonalcoholic fatty liver disease (NAFLD). In fact, NAFLD is often associated with adipocyte enlargement and consequent macrophage recruitment and inflammation. Macrophage polarization is often associated with the proinflammatory state in adipose tissue. In particular, an increase of M1 macrophages number or of M1/M2 ratio triggers the production and secretion of various proinflammatory signals (i.e., adipocytokines). Next, these inflammatory factors may reach the liver leading to local M1/M2 macrophage polarization and consequent onset of the histological damage characteristic of NAFLD. Thus, the role of macrophage polarization and inflammatory signals appears to be central for pathogenesis and progression of NAFLD, even if the heterogeneity of macrophages and molecular mechanisms that govern their phenotype switch remain incompletely understood. In this review, we discuss the role of adipose and liver tissue macrophage-mediated inflammation in experimental and human NAFLD. This focus is relevant because it may help researchers that approach clinical and experimental studies on this disease advancing the knowledge of mechanisms that could be targeted in order to revert NAFLD-related fibrosis.
authors.affiliation: Liver Research Unit of Bambino Gesù Children's Hospital and IRCCS, Rome, Italy.
authors.forename: Anna
authors.identifier: 0000-0001-7241-6329
authors.initials: A
authors.lastname: Alisi
authors.affiliation: Department of Movement, Human and Health Sciences, Division of Health Sciences, University of Rome "Foro Italico", Rome, Italy.
authors.forename: Guido
authors.initials: G
authors.lastname: Carpino
authors.affiliation: Federal University of Rio de Janeiro, Institute of Biomedical Sciences, Rio de Janeiro, Brazil.
authors.forename: Felipe L
authors.initials: FL
authors.lastname: Oliveira
authors.affiliation: Liver Research Unit of Bambino Gesù Children's Hospital and IRCCS, Rome, Italy.
authors.forename: Nadia
authors.initials: N
authors.lastname: Panera
authors.affiliation: Hepato-Metabolic Disease Unit of Bambino Gesù Children's Hospital and IRCCS, Rome, Italy.
authors.forename: Valerio
authors.identifier: 0000-0002-4570-3979
authors.initials: V
authors.lastname: Nobili
authors.affiliation: Department of Anatomical, Histological, Forensic Medicine and Orthopedics Sciences, Sapienza University of Rome, Rome, Italy.
authors.forename: Eugenio
authors.identifier: 0000-0001-6180-3091
authors.initials: E
authors.lastname: Gaudio
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000378:metabolism; D054392:Adipokines / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D005355:Fibrosis; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D018836:Inflammation Mediators; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D065626:Non-alcoholic Fatty Liver Disease / Q000378:metabolism* / Q000473:pathology; D009765:Obesity / Q000378:metabolism; D010641:Phenotype
chemical_list: D054392:Adipokines; D018836:Inflammation Mediators