By Jennifer I. Lim (ed.)
Addressing a big affecting thousands all over the world, this resource compiles the main functional and groundbreaking examine at the etiology, review, and remedy of Age-Related Macular Degeneration (AMD). With full-color illustrations all through, this reference explores learn developments that experience ended in novel treatments that supply sight saving, much less damaging types of therapy for exudative AMD, in addition to concepts to avoid the development of non-exudative AMD. With 3 new chapters and expansive quantity of part updates, this resource provides the newest reports on OCT imaging, experimental remedies, new functions for thermal lasers, and gene treatment for AMD. The resource additionally summarizes reports from present scientific trials to stay the choicest within the provision of deal with sufferers with this disabling disorder.
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Additional info for Age-Related Macular Degeneration
Recruitment of blood-derived reparative macrophages develops early in the course of glomerulosclerosis in proportion to the severity of the injury (151,152). Various innate injury stimuli, including renal hypertension, hyperlipidemia, and glomerular capillary endothelial injury by oxidized LDL, can upregulate macrophage chemotactic factors and adhesion molecules in the capillaries to induce macrophage recruitment (156–158). Experimental data suggest that reparative macrophages release mediators that induce mesangial cell proliferation, amplify the accumulation of extracellular matrix and might induce killing of endothelial cells.
Thus, various immune mechanisms implicated in atherosclerosis might be relevant to AMD. Innate Mechanisms Injury and Atherosclerosis The response to injury hypothesis for the initiation and progression of atherosclerosis has been supported by numerous investigators who cite many different participating injury stimuli (101,108,109). For example, hemodynamic injury by blood ﬂow turbulence can directly injure endothelial cells at bifurcations of major vessels (113). , angiotensin II or endothelin-1) can stimulate the endothelial and smooth muscle responses.
Abbreviations: LPS, lippopolysacccharide; MBL, mannose-binding lectin; MAC, membrane attack complex. classical pathway (10–13). Recently, a new innate activational pathway, the lectin pathway, has been identiﬁed (14). This pathway utilizes mannosebinding lectin (MBL) to recognize sugar moieties, such as mannose and N-acetylglucosamine, on cell surfaces. While MBL does not normally recognize the body’s own tissue, oxidant injury, as can occur in AMD, may alter surface protein expression and glycosylation causing MBL deposition and complement activation (15–18).