Molecular Mechanisms of Kidney Injury and Repair.
acute kidney injury
cell death
chronic kidney disease
kidney
molecular mechanisms
regeneration
treatment
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
28 Jan 2022
28 Jan 2022
Historique:
received:
08
01
2022
revised:
24
01
2022
accepted:
26
01
2022
entrez:
15
2
2022
pubmed:
16
2
2022
medline:
17
3
2022
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 35163470
pii: ijms23031542
doi: 10.3390/ijms23031542
pmc: PMC8835923
pii:
doi:
Substances chimiques
Biomarkers
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Instituto de Salud Carlos III
ID : PI17/01411, PI17/00119, PI18/01366, PI19/00588, PI19/00815, DTS18/00032, PI20/00140
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