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The American Journal of Pathology|August 16, 2011
Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathwayTom Nijenhuis, Alexis J Sloan, Joost G J Hoenderop, et al.
JCI Insight|April 10, 2023
suPAR links a dysregulated immune response to tissue inflammation and sepsis-induced acute kidney injuryChristian Nusshag, Changli Wei, Eunsil Hahm, et al.
The Journal of Clinical Endocrinology and Metabolism|April 18, 2024
Obesity, Inflammation, and Clinical Outcomes in COVID-19: A Multicenter Prospective Cohort StudyChristina G Hutten, Kishan Padalia, Alexi Vasbinder, et al.
Journal of the American Society of Nephrology : JASN|July 26, 2020
Podocyte Integrin-β3 and Activated Protein C Coordinately Restrict RhoA Signaling and Ameliorate Diabetic NephropathyThati Madhusudhan, Sanchita Ghosh, Hongjie Wang, et al.
Biorxiv : the Preprint Server for Biology|August 30, 2024
CD11b suppresses TLR7-driven inflammatory signaling to protect against lupus nephritisXiaobo Li, Veronica Villanueva, Viviana Jimenez, et al.
Nature Medicine|May 12, 2015
Pharmacological targeting of actin-dependent dynamin oligomerization ameliorates chronic kidney disease in diverse animal modelsMario Schiffer, Beina Teng, Changkyu Gu, et al.
The Journal of Clinical Investigation|February 8, 2019
uPAR isoform 2 forms a dimer and induces severe kidney disease in miceChangli Wei, Jing Li, Brian D Adair, et al.
Kidney International|March 14, 2018
Single-nephron proteomes connect morphology and function in proteinuric kidney diseaseMartin Höhne, Christian K Frese, Florian Grahammer, et al.
JAMA Pediatrics|September 6, 2017
Association of Serum Soluble Urokinase Receptor Levels With Progression of Kidney Disease in ChildrenFranz Schaefer, Howard Trachtman, Elke Wühl, et al.
ACS Chemical Biology|November 20, 2018
DNA-Encoded Library-Derived DDR1 Inhibitor Prevents Fibrosis and Renal Function Loss in a Genetic Mouse Model of Alport SyndromeHans Richter, Alexander L Satz, Marc Bedoucha, et al.
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