Regulation of the Actin Cytoskeleton in Podocytes
Autor: | James Dylewski, Judith Blaine |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
podocyte actin cytoskeleton 030232 urology & nephrology Podocyte foot Review macromolecular substances Podocyte Focal adhesion 03 medical and health sciences 0302 clinical medicine medicine foot process Animals Humans Disease focal adhesion lcsh:QH301-705.5 Actin Focal Adhesions Chemistry Podocytes Glomerular basement membrane General Medicine Actin cytoskeleton Actins Cell biology slit diaphragm 030104 developmental biology medicine.anatomical_structure lcsh:Biology (General) Mutation Glomerular Filtration Barrier Slit diaphragm |
Zdroj: | Cells, Vol 9, Iss 1700, p 1700 (2020) Cells |
ISSN: | 2073-4409 |
Popis: | Podocytes are an integral part of the glomerular filtration barrier, a structure that prevents filtration of large proteins and macromolecules into the urine. Podocyte function is dependent on actin cytoskeleton regulation within the foot processes, structures that link podocytes to the glomerular basement membrane. Actin cytoskeleton dynamics in podocyte foot processes are complex and regulated by multiple proteins and other factors. There are two key signal integration and structural hubs within foot processes that regulate the actin cytoskeleton: the slit diaphragm and focal adhesions. Both modulate actin filament extension as well as foot process mobility. No matter what the initial cause, the final common pathway of podocyte damage is dysregulation of the actin cytoskeleton leading to foot process retraction and proteinuria. Disruption of the actin cytoskeleton can be due to acquired causes or to genetic mutations in key actin regulatory and signaling proteins. Here, we describe the major structural and signaling components that regulate the actin cytoskeleton in podocytes as well as acquired and genetic causes of actin dysregulation. |
Databáze: | OpenAIRE |
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