Fibrosis in Chronic Kidney Disease: Pathogenesis and Consequences

作者：Sara Panizo, Laura Martínez‐Arias, Cristina Alonso‐Montes, Pablo Cannata, Beatriz Martín-Carro, José Luis Fernández Martín, Manuel Naves Díaz, Natalia Carrillo‐López, Jorge Benito Cannata-Andía · 发表于：International Journal of Molecular Sciences · 年份：2021 · DOI：10.3390/ijms22010408 · 被引用次数：377 · 研究领域：Parathyroid Disorders and Treatments、Apelin-related biomedical research、Connective Tissue Growth Factor Research

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.