Changli (David) Wei to Glomerulosclerosis, Focal Segmental
This is a "connection" page, showing publications Changli (David) Wei has written about Glomerulosclerosis, Focal Segmental.
Connection Strength
0.834
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The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5. Kidney Int. 2023 06; 103(6):1056-1062.
Score: 0.221
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Podocytes exhibit a specialized protein quality control employing derlin-2 in kidney disease. Am J Physiol Renal Physiol. 2018 03 01; 314(3):F471-F482.
Score: 0.154
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Bone marrow-derived immature myeloid cells are a main source of circulating suPAR contributing to proteinuric kidney disease. Nat Med. 2017 01; 23(1):100-106.
Score: 0.144
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Recurrent Primary Focal Segmental Glomerulosclerosis Managed With Intensified Plasma Exchange and Concomitant Monitoring of Soluble Urokinase-Type Plasminogen Activator Receptor-Mediated Podocyte ?3-integrin Activation. Transplantation. 2015 Dec; 99(12):2593-7.
Score: 0.134
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Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy. Transplantation. 2013 Oct 15; 96(7):649-56.
Score: 0.116
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TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet. 2005 Jul; 37(7):739-44.
Score: 0.065