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Badania genetyczne i komórkowe podocytów w FSGS
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ISBN10: 6209382509
ISBN13: 9786209382505
Publisher: Wydawnictwo Nasza Wiedza
Published: Dec 16 2025
Pages: 120
Weight: 0.38
Height: 0.28 Width: 6.00 Depth: 9.00
Language: Polish
ISBN13: 9786209382505
Publisher: Wydawnictwo Nasza Wiedza
Published: Dec 16 2025
Pages: 120
Weight: 0.38
Height: 0.28 Width: 6.00 Depth: 9.00
Language: Polish
Podocyty tworzą zewnętrzną warstwę bariery filtracyjnej, zapobiegającej wyciekaniu albuminy. Uszkodzenie podocytów prowadzi do ogniskowego segmentowego stwardnienia klębuszków nerkowych (FSGS), będącego glówną przyczyną przewleklej choroby nerek. Przeprowadzilem analizę genetyczną pacjentów z rodzinnym i sporadycznym FSGS oraz zbadalem rolę cytoszkieletu aktynowego w podocytach. Zidentyfikowaliśmy nowy gen podatności na FSGS, ARHGAP24, i wykazaliśmy, że ulegl on mutacji w rodzinie z FSGS. Moje badania sugerują, że równowaga między Rac i Rho może miec znaczenie w FSGS. Wykorzystując indukowalny model myszy transgenicznej i mikroskopię wielofotonową in vivo, potwierdziliśmy, że wysoka aktywnośc Rac1 jest odpowiedzialna za zanik procesów stóp podocytów, zwiększoną dynamikę blony komórkowej i wydzielanie podocytów do moczu, co może prowadzic do bialkomoczu i FSGS. Poprzez sekwencjonowanie dużej grupy pacjentów ze sporadycznym FSGS oraz wykorzystanie nowatorskiego modelu myszy z indukowalnym RNAi specyficznym dla podocytów, który opracowalem, potwierdziliśmy cztery nowe geny, które mogą przyczyniac się do FSGS. Niektóre z tych genów pelnią funkcję regulatorów cytoszkieletu aktynowego. Nasze badania genetyczne potwierdzają rolę regulacji cytoszkieletu aktynowego w patogenezie FSGS.
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