By I. Lim Jennifer
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Additional info for Age-Related Macular Degeneration, 2nd Edition
The activation of complement is also regulated by inhibitors, such as decay accelerating factor, factor H and others which serve to block, resist, or modulate the induction of various activation pathways (7–9). As will be discussed below, the role of complement factor H (CFH) in particular may have critical relevance for AMD. Each activation pathways results in the generation of the same complement byproducts which amplify injury or inﬂammation by at least three mechanisms: (i) a speciﬁc fragment of the third component, C3b, can coat antigenic or pathogenic surfaces in order to enhance phagocytosis by macrophages or neutrophils; (ii) activation of terminal complement components C5–C9, called the membrane attack complex (MAC), forms pores or leaky patches in cell membranes leading to activation of the cell, entrance of extracellular chemicals, loss of cytoplasm or lysis of the cell; and (iii) generation of small pro-inﬂammatory polypeptides, called anaphylatoxins (C3a, C4a, and C5a), can induce many inﬂammatory mediators and lead to the recruitment of inﬂammatory cells.
The pathology of atherosclerosis suggests a spectrum of changes whose pathogenesis may be relevant to the understanding of AMD (107,108). The fatty streak, representing the earliest phase of atherosclerosis, is characterized by lipid deposition and macrophage inﬁltration within the vessel wall (101,108,109). Some investigators have suggested similarities in pathogenesis between fatty streak formation and early AMD (110). The fatty streak can progress into the ﬁbrous plaque, characterized by the proliferation of smooth muscle cells, increasing inﬂammation, and formation of connective tissue with neovascularization within the vessel wall.
Source: From Refs. 146, 147. capillaries and epithelial cells. If enough glomeruli are involved, renal impairment occurs. In some ways, glomerulosclerosis resembles geographic atrophy in AMD (Fig. 6). The response to injury hypothesis has been thoroughly evaluated for renal hypertension, a major cause of glomerulosclerosis (141–145,148). The hemodynamic injury hypothesis proposes that glomerular capillary hypertension causes excessive ﬂow through the glomerulus or hydraulic stretching of the capillary wall to activate injury responses in glomerular cells.