Yet, existing approaches to ECM-producing renal cell population targeting remain controversial, due to the nonspecific expression of currently used markers such as Acta2, Col1a1 and Vim 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22. Since existing therapeutic options remain merely supportive 6 and advanced CKD might result in end-stage kidney disease (ESKD) requiring lifelong dialysis or transplant 7, mechanistic understanding of kidney fibrosis is paramount.Īberrant injury induced fibroblast activation and appearance of myofibroblasts is a crucial pathologic contributor to kidney fibrosis 8, 9, 10, 11. While early fibrotic response is essential for injury recovery 4, excessive extracellular matrix (ECM) production leads to renal parenchymal fibrotic remodeling 5. Similar content being viewed by othersįibrosis is a key underlying process in CKD, resulting in a progressive functional decline with high prevalence, morbidity and mortality 1, 2, 3. Our findings might advance understanding of and targeted intervention in fibrotic kidney disease. We also found that long-term kidney injuries activated a prominent nephrogenic signature, including Sox4 and Hox gene elevation, which prevailed in the distal tubular segments. Moreover, we identified that both models exhibited robust and previously unrecognized distal spatial pattern of TEC injury, outlined by persistent elevation of renal TEC injury markers including Krt8 and Vcam1, while the surviving proximal tubules (PTs) showed restored transcriptional signature. Notably, frTECs shared transcriptional identity with distal nephron segments of the embryonic kidney. Also, both injuries generated failed repair TECs (frTECs) characterized by decline of mature epithelial markers and elevation of stromal and injury markers. We dissected the molecular and cellular landscapes of kidney stroma and newly identified three distinctive fibroblast clusters with “secretory”, “contractile” and “vascular” transcriptional enrichments. Here, we analyzed single cell transcriptomic profiles of two clinically relevant kidney fibrosis models which induced robust kidney parenchymal remodeling. However, cellular and transcriptional landscapes of CKD and specific activated kidney fibroblast clusters remain elusive. Persistent fibroblast activation and tubular epithelial cell (TEC) injury are key CKD contributors. Should you have any product questions or concerns, please visit our Customer Care Portal where you can find knowledgebase articles or chat with a Customer Care Representative using our Live Chat feature.Examining kidney fibrosis is crucial for mechanistic understanding and developing targeted strategies against chronic kidney disease (CKD). To uninstall the ByePass browser extension please click here. Uninstalling the ByePass Browser Extension Your iolo product is now uninstalled and may require a restart of the computer if prompted.
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |