title: Impact of systemic inflammation and autoimmune diseases on apoA-I and HDL plasma levels and functions.
abstract: The cholesterol of high-density lipoproteins (HDLs) and its major proteic component, apoA-I, have been widely investigated as potential predictors of acute cardiovascular (CV) events. In particular, HDL cholesterol levels were shown to be inversely and independently associated with the risk of acute CV diseases in different patient populations, including autoimmune and chronic inflammatory disorders. Some relevant and direct anti-inflammatory activities of HDL have been also recently identified targeting both immune and vascular cell subsets. These studies recently highlighted the improvement of HDL function (instead of circulating levels) as a promising treatment strategy to reduce inflammation and associated CV risk in several diseases, such as systemic lupus erythematosus and rheumatoid arthritis. In these diseases, anti-inflammatory treatments targeting HDL function might improve both disease activity and CV risk. In this narrative review, we will focus on the pathophysiological relevance of HDL and apoA-I levels/functions in different acute and chronic inflammatory pathophysiological conditions.
authors.affiliation: Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 4 rue Gabrielle Perret-Gentil, 1211, Geneva, Switzerland.
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Montecucco
authors.forename: Elda
authors.initials: E
authors.lastname: Favari
authors.forename: Giuseppe Danilo
authors.initials: GD
authors.lastname: Norata
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Ronda
authors.forename: Jerzy-Roch
authors.initials: JR
authors.lastname: Nofer
authors.forename: Nicolas
authors.initials: N
authors.lastname: Vuilleumier
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000097:blood* / Q000737:chemistry; D001327:Autoimmune Diseases / Q000097:blood* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000097:blood* / Q000276:immunology; D008075:Lipoproteins, HDL / Q000097:blood* / Q000737:chemistry; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism; D008246:Lysophospholipids / Q000097:blood; D021962:Membrane Microdomains / Q000276:immunology / Q000378:metabolism; D011487:Protein Conformation; D049349:Receptors, Lysosphingolipid / Q000097:blood; D013110:Sphingosine / Q000031:analogs & derivatives / Q000097:blood; D013329:Structure-Activity Relationship
chemical_list: C505693:APOA1 protein, human; D016632:Apolipoprotein A-I; D015415:Biomarkers; D008075:Lipoproteins, HDL; D008246:Lysophospholipids; D049349:Receptors, Lysosphingolipid; C060506:sphingosine 1-phosphate; D013110:Sphingosine