Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment
Apoptosis plays an important role in many developmental processes and contributes to cell and tissue homeostasis. Induction of apoptosis can involve the "intrinsic pathway", which is activated by diverse stress signals, and the "extrinsic pathway", which is activated by proapoptotic receptor signals...
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| Formato: | Online |
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| Idioma: | inglês |
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Exon Publications
2024
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| Acesso em linha: | https://directory.doabooks.org/handle/20.500.12854/136655 |
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| description | Apoptosis plays an important role in many developmental processes and contributes to cell and tissue homeostasis. Induction of apoptosis can involve the "intrinsic pathway", which is activated by diverse stress signals, and the "extrinsic pathway", which is activated by proapoptotic receptor signals at the cell surface. Excessive or aberrant apoptosis is a crucial factor in many human disorders, including polycystic kidney disease (PKD). Renal cyst formation is caused by dysregulation of cell proliferation, involving diverse and poorly understood molecular mechanisms. Elevated apoptosis of tubular epithelial cells has been described in autosomal dominant PKD (ADPKD) and autosomal recessive PKD (ARPKD), as well as in animal models of PKD. It has been suggested that the dysregulation of apoptosis contributes to cystogenesis of PKD and is associated with the progressive loss of normal nephrons. Inhibition of apoptosis has been shown to delay renal cyst growth in some animal models of PKD. However, increased apoptosis is not a feature in cystic kidneys from Pkd1 mutant mice and inducing apoptosis of the cystic epithelial cells by activation of intrinsic or extrinsic signaling pathways has been shown to slow disease progression with or without inhibition of proliferation. In this chapter, we discuss the positive and negative roles of apoptosis in PKD and the associated molecular mechanisms in regulating cystic renal epithelial cell apoptosis during cyst development. |
| format | Online |
| id | doab-20.500.12854ir-136655 |
| institution | Directory of Open Access Books |
| language | eng |
| publishDate | 2024 |
| publishDateRange | 2024 |
| publishDateSort | 2024 |
| publisher | Exon Publications |
| publisherStr | Exon Publications |
| record_format | ojs |
| spelling | doab-20.500.12854ir-1366552024-05-02T07:42:57Z Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment apoptosis, caspases, cystogenesis, mitochondrial pathway, polycystic kidney disease, proliferation M Apoptosis plays an important role in many developmental processes and contributes to cell and tissue homeostasis. Induction of apoptosis can involve the "intrinsic pathway", which is activated by diverse stress signals, and the "extrinsic pathway", which is activated by proapoptotic receptor signals at the cell surface. Excessive or aberrant apoptosis is a crucial factor in many human disorders, including polycystic kidney disease (PKD). Renal cyst formation is caused by dysregulation of cell proliferation, involving diverse and poorly understood molecular mechanisms. Elevated apoptosis of tubular epithelial cells has been described in autosomal dominant PKD (ADPKD) and autosomal recessive PKD (ARPKD), as well as in animal models of PKD. It has been suggested that the dysregulation of apoptosis contributes to cystogenesis of PKD and is associated with the progressive loss of normal nephrons. Inhibition of apoptosis has been shown to delay renal cyst growth in some animal models of PKD. However, increased apoptosis is not a feature in cystic kidneys from Pkd1 mutant mice and inducing apoptosis of the cystic epithelial cells by activation of intrinsic or extrinsic signaling pathways has been shown to slow disease progression with or without inhibition of proliferation. In this chapter, we discuss the positive and negative roles of apoptosis in PKD and the associated molecular mechanisms in regulating cystic renal epithelial cell apoptosis during cyst development. Published 2024-05-02T07:42:47Z 2024-05-02T07:42:47Z 2015-11-18 chapter 978-0-9944381-0-2 https://directory.doabooks.org/handle/20.500.12854/136655 eng image/jpeg Attribution-NonCommercial-NoDerivatives 4.0 International https://exonpublications.com/index.php/exon/article/view/77 Exon Publications 10.15586/codon.pkd.2015.ch9 10.15586/codon.pkd.2015.ch9 2d6001a3-9e06-4979-bf02-6974e313eb24 978-0-9944381-0-2 197-230 Brisbane(AU) open access |
| spellingShingle | apoptosis, caspases, cystogenesis, mitochondrial pathway, polycystic kidney disease, proliferation M Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title | Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title_full | Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title_fullStr | Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title_full_unstemmed | Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title_short | Apoptosis in Polycystic Kidney Disease: From Pathogenesis to Treatment |
| title_sort | apoptosis in polycystic kidney disease from pathogenesis to treatment |
| topic | apoptosis, caspases, cystogenesis, mitochondrial pathway, polycystic kidney disease, proliferation M |
| topic_facet | apoptosis, caspases, cystogenesis, mitochondrial pathway, polycystic kidney disease, proliferation M |
| url | https://directory.doabooks.org/handle/20.500.12854/136655 |