Ping Zhang
Baylor College of Medicine
10 Papers
55 Citations
Ping Zhang is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Inflammation & Kidney. The author has an hindex of 7, co-authored 10 publications.
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Papers
Stanniocalcin-1 regulates endothelial gene expression and modulates transendothelial migration of leukocytes
Arup Chakraborty,Heddwen L. Brooks,Ping Zhang,Wayne Smith,Matthew R. McReynolds,Jay B. Hoying,Roger J. Bick,Luan D. Truong,Brian J. Poindexter,Hui Lan,Wafa M. Elbjeirami,David Sheikh-Hamad +11 more
TL;DR: The data suggest that STC1 plays a critical role in transendothelial migration of inflammatory cells and is involved in the regulation of numerous aspects of endothelial function.
62
Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis
Gabriela Garcia,Luan D. Truong,Luan D. Truong,Ping Li,Ping Zhang,Richard J. Johnson,Curtis B. Wilson,Lili Feng +7 more
TL;DR: It is concluded that CXCL16/CXCR6 plays a critical role in stimulating leukocyte influx, which causes glomerular damage during anti-GBM glomerulonephritis even when the disease is established.
Adenosine A2A receptor activation and macrophage-mediated experimental glomerulonephritis
TL;DR: Protection against acute and chronic inflammation was associated with suppression of the glomerular expression of the MDC/CCL22 chemokine and down‐regulation of MIP‐1α/CCCL3, RANTES/ CCL5, Mip‐1β/CC L4, and MCP‐1/CCl2 chemokines.
54
Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7
TL;DR: The results show that potassium supplementation can reduce renal inflammation and hence, could modulate the progression of kidney injury in CKD.
51
AT1A-mediated activation of kidney JNK1 and SMAD2 in obstructive uropathy: preservation of kidney tissue mass using candesartan.
Ann M Wamsley-Davis,Ranjit S. Padda,Luan D. Truong,Chun Chui Tsao,Ping Zhang,David Sheikh-Hamad +5 more
TL;DR: The renoprotective effects afforded by AT(1A)-receptor blockade in obstructive uropathy are consistent with attenuation of JNK1- and SMAD2-mediated renal injury.