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A szem struktúráit vérrel ellátó érendothelium működészavarának kulcsfontosságú a szerepe az időskori maculadegeneráció létrejöttében, és indirekt bizonyítékok arra utalnak, hogy az időskori maculadegeneráció érbetegség, végső soron az egész érrendszer megbetegedésének a része. Az ártalmak, a rizikófaktorok oxidatív stresszhez vezetnek, ami aktiválja az endothelt, és szövetkárosodás alakul ki. Az erek, így a szem érhártyájában, a chorioideában lévő erek falát is számos ismétlődő és/vagy elhúzódó inger éri, amelyek mechanikai, fizikai, kémiai, mikrobiológiai, immunológiai, illetve genetikai eredetűek lehetnek. Bármilyen hosszan tartó/ismétlődő ártalom, amely működésbe hozza a védekezés láncreakcióját, gyulladást vált ki. Az ártalmas behatás eliminálásának sikertelensége endothelműködés-zavart, ér/szövet károsodást, időskori maculadegenerációt eredményez(het). Mindezek a tények arra utalnak, hogy az időskori maculadegeneráció érbetegség, az egész érrendszer megbetegedésének a része. Ami a kockázati tényezők jelenlétében kialakuló endotheldiszfunkció és következményes időskori maculadegeneráció kiküszöbölésének, megelőzésének, illetve megszüntetésének stratégiáját illeti, számos jótékony nem gyógyszeres és farmakológiai intervenció áll rendelkezésre: joggal várható, hogy az endotheldiszfunkció helyreállítása megakadályozza az érbántalom és így az időskori maculadegeneráció kialakulását vagy csökkenti a már kialakult elváltozást. Orv. Hetil., 2015, 156(9), 358–365.

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