Age-Related Macular Degeneration, 2nd Edition by I. Lim Jennifer

By I. Lim Jennifer

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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.

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