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Molecular Mechanisms of Kidney Injury and Repair

Chronic kidney disease (CKD) will become the fifth global cause of death by 2040, thus emphasizing the need to better understand the molecular mechanisms of damage and regeneration in the kidney. CKD predisposes to acute kidney injury (AKI) which, in turn, promotes CKD progression. This implies that...

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Autores principales: Rayego-Mateos, Sandra, Marquez-Expósito, Laura, Rodrigues-Diez, Raquel, Sanz, Ana B., Guiteras, Roser, Doladé, Nuria, Rubio-Soto, Irene, Manonelles, Anna, Codina, Sergi, Ortiz, Alberto, Cruzado, Josep M., Ruiz-Ortega, Marta, Sola, Anna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835923/
https://www.ncbi.nlm.nih.gov/pubmed/35163470
http://dx.doi.org/10.3390/ijms23031542
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author Rayego-Mateos, Sandra
Marquez-Expósito, Laura
Rodrigues-Diez, Raquel
Sanz, Ana B.
Guiteras, Roser
Doladé, Nuria
Rubio-Soto, Irene
Manonelles, Anna
Codina, Sergi
Ortiz, Alberto
Cruzado, Josep M.
Ruiz-Ortega, Marta
Sola, Anna
author_facet Rayego-Mateos, Sandra
Marquez-Expósito, Laura
Rodrigues-Diez, Raquel
Sanz, Ana B.
Guiteras, Roser
Doladé, Nuria
Rubio-Soto, Irene
Manonelles, Anna
Codina, Sergi
Ortiz, Alberto
Cruzado, Josep M.
Ruiz-Ortega, Marta
Sola, Anna
author_sort Rayego-Mateos, Sandra
collection PubMed
description Chronic kidney disease (CKD) will become the fifth global cause of death by 2040, thus emphasizing the need to better understand the molecular mechanisms of damage and regeneration in the kidney. CKD predisposes to acute kidney injury (AKI) which, in turn, promotes CKD progression. This implies that CKD or the AKI-to-CKD transition are associated with dysfunctional kidney repair mechanisms. Current therapeutic options slow CKD progression but fail to treat or accelerate recovery from AKI and are unable to promote kidney regeneration. Unraveling the cellular and molecular mechanisms involved in kidney injury and repair, including the failure of this process, may provide novel biomarkers and therapeutic tools. We now review the contribution of different molecular and cellular events to the AKI-to-CKD transition, focusing on the role of macrophages in kidney injury, the different forms of regulated cell death and necroinflammation, cellular senescence and the senescence-associated secretory phenotype (SAPS), polyploidization, and podocyte injury and activation of parietal epithelial cells. Next, we discuss key contributors to repair of kidney injury and opportunities for their therapeutic manipulation, with a focus on resident renal progenitor cells, stem cells and their reparative secretome, certain macrophage subphenotypes within the M2 phenotype and senescent cell clearance.
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spelling pubmed-88359232022-02-12 Molecular Mechanisms of Kidney Injury and Repair Rayego-Mateos, Sandra Marquez-Expósito, Laura Rodrigues-Diez, Raquel Sanz, Ana B. Guiteras, Roser Doladé, Nuria Rubio-Soto, Irene Manonelles, Anna Codina, Sergi Ortiz, Alberto Cruzado, Josep M. Ruiz-Ortega, Marta Sola, Anna Int J Mol Sci Review Chronic kidney disease (CKD) will become the fifth global cause of death by 2040, thus emphasizing the need to better understand the molecular mechanisms of damage and regeneration in the kidney. CKD predisposes to acute kidney injury (AKI) which, in turn, promotes CKD progression. This implies that CKD or the AKI-to-CKD transition are associated with dysfunctional kidney repair mechanisms. Current therapeutic options slow CKD progression but fail to treat or accelerate recovery from AKI and are unable to promote kidney regeneration. Unraveling the cellular and molecular mechanisms involved in kidney injury and repair, including the failure of this process, may provide novel biomarkers and therapeutic tools. We now review the contribution of different molecular and cellular events to the AKI-to-CKD transition, focusing on the role of macrophages in kidney injury, the different forms of regulated cell death and necroinflammation, cellular senescence and the senescence-associated secretory phenotype (SAPS), polyploidization, and podocyte injury and activation of parietal epithelial cells. Next, we discuss key contributors to repair of kidney injury and opportunities for their therapeutic manipulation, with a focus on resident renal progenitor cells, stem cells and their reparative secretome, certain macrophage subphenotypes within the M2 phenotype and senescent cell clearance. MDPI 2022-01-28 /pmc/articles/PMC8835923/ /pubmed/35163470 http://dx.doi.org/10.3390/ijms23031542 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Rayego-Mateos, Sandra
Marquez-Expósito, Laura
Rodrigues-Diez, Raquel
Sanz, Ana B.
Guiteras, Roser
Doladé, Nuria
Rubio-Soto, Irene
Manonelles, Anna
Codina, Sergi
Ortiz, Alberto
Cruzado, Josep M.
Ruiz-Ortega, Marta
Sola, Anna
Molecular Mechanisms of Kidney Injury and Repair
title Molecular Mechanisms of Kidney Injury and Repair
title_full Molecular Mechanisms of Kidney Injury and Repair
title_fullStr Molecular Mechanisms of Kidney Injury and Repair
title_full_unstemmed Molecular Mechanisms of Kidney Injury and Repair
title_short Molecular Mechanisms of Kidney Injury and Repair
title_sort molecular mechanisms of kidney injury and repair
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835923/
https://www.ncbi.nlm.nih.gov/pubmed/35163470
http://dx.doi.org/10.3390/ijms23031542
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