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.
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