Focal segmental glomerulosclerosis; why does it occur segmentally?
Autor: | Satoshi Hara, Michio Nagata, Namiko Kobayashi |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Pathology Physiology Clinical Biochemistry 030232 urology & nephrology urologic and male genital diseases Podocyte 03 medical and health sciences 0302 clinical medicine Focal segmental glomerulosclerosis Physiology (medical) Internal medicine medicine Animals Humans Glomerular disease Hyaline Sclerosis urogenital system business.industry Glomerulosclerosis Focal Segmental Podocytes Microangiopathy Glomerulosclerosis Protein leakage medicine.disease Molecular medicine female genital diseases and pregnancy complications 030104 developmental biology medicine.anatomical_structure Endocrinology business |
Zdroj: | Pflugers Archiv : European journal of physiology. 469(7-8) |
ISSN: | 1432-2013 |
Popis: | Podocyte loss is the fundamental basis of glomerulosclerosis. Focal segmental glomerulosclerosis (FSGS) is a progressive glomerular disease, and its glomerular features are a prototype of podocyte loss-driven glomerulosclerosis. The glomerular pathology of FSGS is characterized by a focal and segmental location of the sclerotic lesions in human FSGS; segmental sclerosis often shows simultaneous intra- and extra-capillary changes, including parietal cell migration, capillary collapse, hyaline deposition, and intra-capillary thrombi and occasional hypercellularity. This suggests that local cellular events, initiated by podocyte loss, are the basis of the segmental lesions in FSGS. Using podocyte-specific injury by toxin administration, a series of recent works has identified the cellular basis of the glomerular response to podocyte loss. This review discusses the molecular pathway of the local response to podocyte loss and its progression to sclerosis. Recent results suggest that segmental sclerosis is a physiological tissue response aimed at halting protein leakage from a disrupted filtration barrier. |
Databáze: | OpenAIRE |
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