Investigators showed in rodent models that long-term consumption of a processed diet drives intestinal barrier permeability and an increased risk of chronic kidney disease.
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Snelson, M., Tan, S. M., Clarke, R. E., Pasquale, C. de, Thallas-Bonke, V., Nguyen, T.-V., Penfold, S. A., Harcourt, B. E., Sourris, K. C., Lindblom, R. S., Ziemann, M., Steer, D., El-Osta, A., Davies, M. J., Donnellan, L., Deo, P., Kellow, N. J., Cooper, M. E., Woodruff, T. M., … Coughlan, M. T. (2021). Processed foods drive intestinal barrier permeability and microvascular diseases. Science Advances, 7(14), eabe4841. https://doi.org/10.1126/sciadv.abe4841 Cite
A comprehensive metabolomic study of the response of HK-2 cells, a human cell line derived from normal proximal tubular epithelial cells, to hyperglycemic, hypoxic diabetic-like milieu has been performed.
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Among the 32 neutrophil gelatinase-associated lipocalin (NGAL) inhibitors tested, GPZ614741 and GPZ058225 fully blocked NGAL-induced inflammatory and profibrotic markers in human cardiac fibroblasts and primary mouse kidney fibroblasts.
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Antifibrotic effect of novel neutrophil gelatinase-associated lipocalin inhibitors in cardiac and renal disease models | Scientific Reports. (n.d.). Retrieved January 28, 2021, from https://www.nature.com/articles/s41598-021-82279-0 Cite
This study analyzes the role of uremic toxins in sarcopenia at different stages of chronic kidney disease (CKD), evaluating changes in the muscular regeneration process. Cultured C2C12 cells were incubated with a combination of indoxyl sulphate and p-cresol at high doses or low doses resembling late or early CKD stages, respectively.
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Investigators demonstrated that recessive NOS1AP variants impaired CDC42/DIAPH-dependent actin remodeling, causing aberrant organoid glomerulogenesis, and leading to a glomerulopathy in humans and mice.
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Majmundar, A. J., Buerger, F., Forbes, T. A., Klämbt, V., Schneider, R., Deutsch, K., Kitzler, T. M., Howden, S. E., Scurr, M., Tan, K. S., Krzeminski, M., Widmeier, E., Braun, D. A., Lai, E., Ullah, I., Amar, A., Kolb, A., Eddy, K., Chen, C. H., … Hildebrandt, F. (2021). Recessive NOS1AP variants impair actin remodeling and cause glomerulopathy in humans and mice. Science Advances, 7(1), eabe1386. https://doi.org/10.1126/sciadv.abe1386 Cite
The authors discuss the roles of microRNAs in the pathophysiological mechanisms of vascular calcification in smooth muscle cells and describes several interventions against vascular calcification by regulating microRNAs.
[Journal of Cellular and Molecular Medicine]
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WNT–β-catenin signaling is involved in chronic kidney disease-associated vascular calcification and mineral bone disease. The WNT–β-catenin pathway is tightly regulated, for example, by proteins of the Dickkopf family.
[Nature Reviews Nephrology]
The authors provide a comprehensive overview of the current understanding of fibroblast growth factor (FGF) signaling and its roles in organ development, injury repair, and the pathophysiology of a spectrum of diseases, which is a consequence of FGF signaling dysregulation.
[Signal Transduction and Targeted Therapy]
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Treatment with IL-10+ extracellular vesicles significantly ameliorated renal tubular injury and inflammation caused by ischemia/reperfusion injury, and potently prevented the transition to chronic kidney disease.
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Tang, T.-T., Wang, B., Wu, M., Li, Z.-L., Feng, Y., Cao, J.-Y., Yin, D., Liu, H., Tang, R.-N., Crowley, S. D., Lv, L.-L., & Liu, B.-C. (2020). Extracellular vesicle–encapsulated IL-10 as novel nanotherapeutics against ischemic AKI. Science Advances, 6(33), eaaz0748. https://doi.org/10.1126/sciadv.aaz0748 Cite
Scientists identified the basic biological properties and examined the multilineage differentiation potential of umbilical cord-MSCs.
[Stem Cell Research & Therapy]
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Xiang, E., Han, B., Zhang, Q., Rao, W., Wang, Z., Chang, C., Zhang, Y., Tu, C., Li, C., & Wu, D. (2020). Human umbilical cord-derived mesenchymal stem cells prevent the progression of early diabetic nephropathy through inhibiting inflammation and fibrosis. Stem Cell Research & Therapy, 11(1), 336. https://doi.org/10.1186/s13287-020-01852-y Cite