Cellular Stress and Molecular Responses in Bladder Ischemia

The concept of bladder ischemia as a contributing factor to detrusor overactivity and lower urinary tract symptoms (LUTS) is evolving. Bladder ischemia as a consequence of pelvic arterial atherosclerosis was first documented in experimental models and later in elderly patients with LUTS. It was show...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Jing-Hua Yang, Han-Pil Choi, Wanting Niu, Kazem M. Azadzoi
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	bladder ischemia cellular stress post-translational modifications non-coded amino acids Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/2772dd8bb8104cf186e2eb5ea5998762
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:2772dd8bb8104cf186e2eb5ea5998762
record_format	dspace
spelling	oai:doaj.org-article:2772dd8bb8104cf186e2eb5ea59987622021-11-11T17:17:11ZCellular Stress and Molecular Responses in Bladder Ischemia10.3390/ijms2221118621422-00671661-6596https://doaj.org/article/2772dd8bb8104cf186e2eb5ea59987622021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11862https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067The concept of bladder ischemia as a contributing factor to detrusor overactivity and lower urinary tract symptoms (LUTS) is evolving. Bladder ischemia as a consequence of pelvic arterial atherosclerosis was first documented in experimental models and later in elderly patients with LUTS. It was shown that early-stage moderate ischemia produces detrusor overactivity, while prolonged severe ischemia provokes changes consistent with detrusor underactivity. Recent studies imply a central role of cellular energy sensors, cellular stress sensors, and stress response molecules in bladder responses to ischemia. The cellular energy sensor adenosine monophosphate-activated protein kinase was shown to play a role in detrusor overactivity and neurodegeneration in bladder ischemia. The cellular stress sensors apoptosis signal-regulating kinase 1 and caspase-3 along with heat shock proteins were characterized as important contributing factors to smooth muscle structural modifications and apoptotic responses in bladder ischemia. Downstream pathways seem to involve hypoxia-inducible factor, transforming growth factor beta, vascular endothelial growth factor, and nerve growth factor. Molecular responses to bladder ischemia were associated with differential protein expression, the accumulation of non-coded amino acids, and post-translational modifications of contractile proteins and stress response molecules. Further insight into cellular stress responses in bladder ischemia may provide novel diagnostic and therapeutic targets against LUTS.Jing-Hua YangHan-Pil ChoiWanting NiuKazem M. AzadzoiMDPI AGarticlebladder ischemiacellular stresspost-translational modificationsnon-coded amino acidsBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11862, p 11862 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	bladder ischemia cellular stress post-translational modifications non-coded amino acids Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	bladder ischemia cellular stress post-translational modifications non-coded amino acids Biology (General) QH301-705.5 Chemistry QD1-999 Jing-Hua Yang Han-Pil Choi Wanting Niu Kazem M. Azadzoi Cellular Stress and Molecular Responses in Bladder Ischemia
description	The concept of bladder ischemia as a contributing factor to detrusor overactivity and lower urinary tract symptoms (LUTS) is evolving. Bladder ischemia as a consequence of pelvic arterial atherosclerosis was first documented in experimental models and later in elderly patients with LUTS. It was shown that early-stage moderate ischemia produces detrusor overactivity, while prolonged severe ischemia provokes changes consistent with detrusor underactivity. Recent studies imply a central role of cellular energy sensors, cellular stress sensors, and stress response molecules in bladder responses to ischemia. The cellular energy sensor adenosine monophosphate-activated protein kinase was shown to play a role in detrusor overactivity and neurodegeneration in bladder ischemia. The cellular stress sensors apoptosis signal-regulating kinase 1 and caspase-3 along with heat shock proteins were characterized as important contributing factors to smooth muscle structural modifications and apoptotic responses in bladder ischemia. Downstream pathways seem to involve hypoxia-inducible factor, transforming growth factor beta, vascular endothelial growth factor, and nerve growth factor. Molecular responses to bladder ischemia were associated with differential protein expression, the accumulation of non-coded amino acids, and post-translational modifications of contractile proteins and stress response molecules. Further insight into cellular stress responses in bladder ischemia may provide novel diagnostic and therapeutic targets against LUTS.
format	article
author	Jing-Hua Yang Han-Pil Choi Wanting Niu Kazem M. Azadzoi
author_facet	Jing-Hua Yang Han-Pil Choi Wanting Niu Kazem M. Azadzoi
author_sort	Jing-Hua Yang
title	Cellular Stress and Molecular Responses in Bladder Ischemia
title_short	Cellular Stress and Molecular Responses in Bladder Ischemia
title_full	Cellular Stress and Molecular Responses in Bladder Ischemia
title_fullStr	Cellular Stress and Molecular Responses in Bladder Ischemia
title_full_unstemmed	Cellular Stress and Molecular Responses in Bladder Ischemia
title_sort	cellular stress and molecular responses in bladder ischemia
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/2772dd8bb8104cf186e2eb5ea5998762
work_keys_str_mv	AT jinghuayang cellularstressandmolecularresponsesinbladderischemia AT hanpilchoi cellularstressandmolecularresponsesinbladderischemia AT wantingniu cellularstressandmolecularresponsesinbladderischemia AT kazemmazadzoi cellularstressandmolecularresponsesinbladderischemia
_version_	1718432106549346304

Cellular Stress and Molecular Responses in Bladder Ischemia

Ejemplares similares