Fibrosis in chronic kidney disease: Pathogenesis and consequences

Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of repar...

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Bibliographic Details
Authors: Panizo, Sara, Martínez-Arias, Laura, Alonso-Montes, Cristina, Cannata Ortiz, Pablo Javier, Martín-Carro, Beatriz, Fernández-Martín, José L., Naves-Díaz, Manuel, Carrillo-López, Natalia, Cannata-Andía, Jorge B.
Format: article
Publication Date:2021
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:repositorio.uam.es:10486/698059
Online Access:http://hdl.handle.net/10486/698059
https://dx.doi.org/10.3390/ijms22010408
Access Level:Open access
Keyword:Artificial intelligence
FGF23
Fibrosis
Image analysis
Inflammation
Klotho
MicroRNAs
PTH
RAS
Vitamin D
Medicina
Description
Summary:Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of reparation converging in molecular signals responsible of initiating and driving fibrosis. Though fibrosis can play a defensive role, in several circumstances at a certain stage, it can progressively become an uncontrolled irreversible and self-maintained process, named pathological fibrosis. Several systems, molecules and responses involved in the pathogenesis of the pathological fibrosis of chronic kidney disease (CKD) will be discussed in this review, putting special attention on inflammation, renin-angiotensin system (RAS), parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), Klotho, microRNAs (miRs), and the vitamin D hormonal system. All of them are key factors of the core and regulatory pathways which drive fibrosis, having a great negative kidney and cardiac impact in CKD.

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