Journal
FRONTIERS IN IMMUNOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.611830
Keywords
apoE; C-reactive protein; adiponectin; HDL; amyloid-beta; protein
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Funding
- Jane and Aatos Erkko Foundation [15032019]
- Finnish Foundation for Cardiovascular Research [08042019]
- Academy of Finland [331108]
- Helsinki University Hospital Funds (VTR)
- Academy of Finland (AKA) [331108, 331108] Funding Source: Academy of Finland (AKA)
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Complement-mediated inflammation or dysregulation in lipid metabolism are associated with the pathogenesis of several diseases. These include age-related macular degeneration (AMD), C3 glomerulonephritis (C3GN), dense deposit disease (DDD), atherosclerosis, and Alzheimer's disease (AD). In all these diseases, formation of characteristic lipid-rich deposits is evident. Here, we will discuss molecular mechanisms whereby dysfunction of complement, and especially of its key regulator factor H, could be involved in lipid accumulation and related inflammation. The genetic associations to factor H polymorphisms, the role of factor H in the resolution of inflammation in lipid-rich deposits, modification of macrophage functions, and complement-mediated clearance of apoptotic and damaged cells indicate that the function of factor H is crucial in limiting inflammation in these diseases.
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