Processed Foods Drive Intestinal Barrier Permeability and Microvascular Diseases

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.
[Science Advances]
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
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Comprehensive Metabolomic Study of the Response of HK-2 Cells to Hyperglycemic Hypoxic Diabetic-Like Milieu

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.
[Scientific Reports]
Valdés, A., Lucio-Cazaña, F. J., Castro-Puyana, M., García-Pastor, C., Fiehn, O., & Marina, M. L. (2021). Comprehensive metabolomic study of the response of HK-2 cells to hyperglycemic hypoxic diabetic-like milieu. Scientific Reports, 11(1), 5058. https://doi.org/10.1038/s41598-021-84590-2 Cite
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Antifibrotic Effect of Novel Neutrophil Gelatinase-Associated Lipocalin Inhibitors in Cardiac and Renal Disease Models

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.
[Scientific Reports]
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
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In Vivo Silencing of Amphiregulin by a Novel Effective Self-Assembled-Micelle Inhibitory RNA Ameliorates Renal Fibrosis via Inhibition of EGFR Signals

TGF-β1-induced ECM production and myofibroblast differentiation were attenuated by Amphiregulin-targeting Self-Assembled-Micelle inhibitory RNA (SAMiRNA-AREG). Researchers confirmed that upregulated AREG in the ureteral obstruction or adenine diet models was mainly localized in the distal tubules.
[Scientific Reports]
Son, S. S., Hwang, S., Park, J. H., Ko, Y., Yun, S.-I., Lee, J.-H., Son, B., Kim, T. R., Park, H.-O., & Lee, E. Y. (2021). In vivo silencing of amphiregulin by a novel effective Self-Assembled-Micelle inhibitory RNA ameliorates renal fibrosis via inhibition of EGFR signals. Scientific Reports, 11(1), 2191. https://doi.org/10.1038/s41598-021-81726-2 Cite
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Uremic Toxins Impair Skeletal Muscle Regeneration by Inhibiting Myoblast Proliferation, Reducing Myogenic Differentiation, and Promoting Muscular Fibrosis

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.
[Scientific Reports]
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Recessive NOS1AP Variants Impair Actin Remodeling and Cause Glomerulopathy in Humans and Mice

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.
[Science Advances]
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
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MicroRNAs Are Critical in Regulating Smooth Muscle Cell Mineralization and Apoptosis during Vascular Calcification

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 – A Versatile Player in Kidney Injury and Repair

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]
Schunk, S. J., Floege, J., Fliser, D., & Speer, T. (2020). WNT–β-catenin signalling — a versatile player in kidney injury and repair. Nature Reviews Nephrology, 1–13. https://doi.org/10.1038/s41581-020-00343-w Cite
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FGF/FGFR Signaling in Health and Disease

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]
Xie, Y., Su, N., Yang, J., Tan, Q., Huang, S., Jin, M., Ni, Z., Zhang, B., Zhang, D., Luo, F., Chen, H., Sun, X., Feng, J. Q., Qi, H., & Chen, L. (2020). FGF/FGFR signaling in health and disease. Signal Transduction and Targeted Therapy, 5(1), 1–38. https://doi.org/10.1038/s41392-020-00222-7 Cite
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Adebiyi Awarded $4.5 Million from the NIH for Vascular, Kidney Dysfunction Research

Over the last 10 years, Dr. Adebiyi’s laboratory has focused on investigating cellular mechanisms that control vascular and kidney functions in health and disease of newborns and adults. Dr. Adebiyi recently received two new grants from the National Institutes of Health to support these research initiatives.
[University of Tennessee (EurekaAlert!)]
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Extracellular Vesicle–Encapsulated IL-10 as Novel Nanotherapeutics against Ischemic AKI

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.
[Science Advances]
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
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