The roles of collagen in chronic kidney disease and vascular calcification
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REVIEW
The roles of collagen in chronic kidney disease and vascular calcification Aoran Huang 1 & Guangying Guo 1 & Yanqiu Yu 2,3 & Li Yao 1 Received: 10 July 2020 / Revised: 18 November 2020 / Accepted: 20 November 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract The extracellular matrix component collagen is widely expressed in human tissues and participates in various cellular biological processes. The collagen amount generally remains stable due to intricate regulatory networks, but abnormalities can lead to several diseases. During the development of renal fibrosis and vascular calcification, the expression of collagen is significantly increased, which promotes phenotypic changes in intrinsic renal cells and vascular smooth muscle cells, thereby exacerbating disease progression. Reversing the overexpression of collagen substantially prevents or slows renal fibrosis and vascular calcification in a wide range of animal models, suggesting a novel target for treating patients with these diseases. Stem cell therapy seems to be an effective strategy to alleviate these two conditions. However, recent findings indicate that the natural pore structure of collagen fibers is sufficient to induce the inappropriate differentiation of stem cells and thereby exacerbate renal fibrosis and vascular calcification. A comprehensive understanding of the role of collagen in these diseases and its effect on stem cell biology will assist in improving the unmet requirements for treating patients with kidney disease. Keywords Collagen . Extracellular matrix . Chronic kidney disease . Renal fibrosis . Vascular calcification . Stem cells
Introduction Chronic kidney disease (CKD) is irreversible, has no cure, and is often associated with adverse clinical outcomes. It is estimated that over 800 million individuals might have CKD, with a prevalence between 11 and 13% worldwide, placing an immense burden on the global economy [1]. Renal fibrosis, characterized by excess extracellular matrix protein accumulation, is a typical feature of CKD and represents the final common pathway among all progressive kidney diseases [2]. Patients with renal fibrosis suffer from kidney structure destruction and decreased renal function and eventually develop * Yanqiu Yu [email protected] * Li Yao [email protected] 1
Department of Nephrology, The First Hospital of China Medical University, Shenyang 110000, China
2
Department of Pathophysiology, College of Basic Medical Sciences, China Medical University, Shenyang 110013, China
3
Shenyang Engineering Technology R&D Center of Cell Therapy Co. LTD., Shenyang 110169, China
end-stage renal disease (ESRD), requiring kidney transplantation and dialysis. Fibrosis can occur in any kidney structure, such as the glomeruli, tubular intestine, and renal vasculature, and these conditions are named glomerulosclerosis (GS), tubulointerstitial fibrosis (TIF), and arteriolosclerosis, respectively. Previous studies have identified numerous risk factors associated with renal fibrosis, but the role
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