Nazım DENİZLİ, Yasemin KIRAÇ, Murat GÜCÜN, Recep DEMİRCİ, Murat DURANAY

Podositler ve nefrotik sendrom için yeni tedavi hedefleri

Podositler yüksek diferansiyasyon gösteren hücrelerdir. Podositlerin belki de en önemli komponentleri olan slit diyafram ve onunla ilişkili proteinler (mesela; nefrin, podosin, α3β1 integrin, alfa-aktinin-4 (ACTN4), adaptör protein CD2AP ve TRCP6) ile ayaksı çıkıntıları altındaki glomerüler bazal membrana bağlayan proteinler (mese la; α3β1 integrin, integrin-linked kinaz (ILK) ve tetraspanin CD151 ) podositlerdeki aktin-hücre iskeleti ile bağ kurar lar ve proteinürinin önlenmesinde kritik rol oynarlar. Genellikle podosit slit diyafram ve aktin-hücre iskeleti üzerinde sergilenen podosit hasarı, glomerüler hastalık ların karakteristik özelliğidir. Proteinüri, sık olarak podosit ayaksı çıkıntılarda silinme ve büzüşmelerle karakterize glomerülde ortaya çıkan sitopatolojik değişikliklerle bir liktedir. Podosit ilişkili genetik defektler proteinüri ve fokal segmental glomeruloskleroz (FSGS) ile sonuçlanır lar. Podosit hasar mekanizmalarının iyi anlaşılması, proteinürinin tedavisinde de yeni gelişmeleri beraberinde getirecektir.

Anahtar Kelimeler:

Proteinüri, Anjiyotensin dönüştürücü enzim inhibitörleri, Nefrotik sendrom, Podosit

Podocytes and novel therapeutic targets for nephrotic syndrome

The podocytes are highly differentiated cells. Proteins that are associated with the slit diaphragm (for example, nephrin, podocin, α-actinin-4, the adaptor protein CD2AP, and TRPC6), and those that anchor the foot processes to the glomerular basal membrane (GBM) (for example, α3β1 integrin, integrin-linked kinase (ILK), and the tetraspanin CD151), are connected to the actin cytoskeleton, which has an important role in the prevention of proteinuria. Podocyte and slit diaphragm injury is a hallmark of glomerular disease, which is generally displayed by the rearrangement of the podocyte slit diaphragm and the actin cytoskeleton. Proteinuria is often accompanied by a cytopathological change in the glomerulus that is referred to as effacement of the podocyte foot processes. Podocyte-associated genetic defects result in proteinuria and progression to focal segmental glomerulosclerosis (FSGS). Understanding of the mechanisms of the podocyte injury will probably reveal novel therapeutic targets for proteinuria.

Keywords:

Proteinuria, Angiotensin-Converting Enzyme Inhibitors, Nephrotic Syndrome, Podocytes,

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