Cellular and Molecular Basis in Chronic Kidney Disease
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: 25 November 2024 | Viewed by 2227
Special Issue Editor
Special Issue Information
Dear Colleagues,
Chronic kidney disease (CKD) corresponds to a condition involving an alteration in kidney capacity persisting for three months or more with eventual loss of function over time. CKD can be divided into five specific stages, with factors such as glomerular filtration rate (GFR) and albuminuria serving as criteria for categorization. One of the central pathways involved in the pathogenesis of CKD is the renin–angiotensin–aldosterone system (RAAS). When this pathway is activated, it induces contraction of the glomerular afferent arterioles, resulting in worsening renal ischemia which ultimately diminishes glomerular filtration capacity. Of the enzymes and peptides involved, aldosterone has been identified as causing pathological effects leading to kidney inflammation and fibrosis. In the CKD model, aldosterone production has been shown to be elevated and involved in the formation of fibroblast cells, renal fibrosis, and initiation of hypertension, all of which cause sodium overload. Collectively, these effects manifest into worsening renal damage. Another fundamental aspect found present in every stage of CKD is renal fibrosis and one important mediator of myofibroblast activation is TGF-B1. Collectively, RAAS, TGF-B1, and other factors such as vascular calcification and uremic toxins are known to be involved in CKD, causing worsening renal inflammation and fibrosis, both of which diminish renal capacity and function. This Special Issue on CKD aims to recruit original papers, reviews, and communication that enhance the understanding of cellular and molecular mechanisms involved in the pathophysiology of CKD.
Dr. Prabhatchandra Dube
Guest Editor
Manuscript Submission Information
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Keywords
- CKD
- renal inflammation
- renal fibrosis
- RAAS
- aldosterone
- TGF-B1
- uremic toxins
- hypertension
- GFR
- albuminuria
