David Salant

Renal Section, Boston University Medical Center, United States of America

David J Salant, MD

Academic positions:
- Prof. of Medicine, Pathology & Lab. Medicine
- Chief, Renal Section, Boston Medical Centre

All industry positions (in last five years):
None declared

Research interests:
The focus of the lab is on the immune basis of glomerular diseases with particular regard to the humoral mechanisms of glomerular cell injury. Current work will elucidate the mechanisms by which antibodies alter the function & morphology of glomerular visceral epithelial cells (podocytes), including the role of podocyte-specific antibodies, & the effects of complement-mediated injury on podocyte structure, composition of the filtration slit diaphragm & its attachment to the cytoskeleton, & on cell-matrix adhesion. Having identified Notch4 protein in rodent glomeruli, we are engaged in studies to elucidate the role of Notch4 in mature podocytes through the use of Notch4 knockout mice & in vitro podocyte expression systems. Efforts are also underway to isolate & identify the membranous nephropathy autoantigen/s on the podocyte plasma membrane of human kidneys using cell fractionation, biochemical purification, immunochemistry, & mass spectroscopy. Animal models are used to elucidate the mechanisms of post-inflammatory fibrogenesis of the kidney & test the therapeutic efficacy & anti-fibrotic agents.

Any other information:
Member of the American Soc. of Nephrology, International Soc. of Nephrology, American Assoc. for Advancement of Science, American Soc. for Clinical Investigation, American Heart Assoc., American Assoc. of Physicians & NIH Study Sections & Special Emphasis Panels.

Any competing interests declared are displayed with individual evaluations.

Faculty Member: Nephrology > Renal Immunology & Pathology (inc. Glomerular Diseases) (since 11 November 2005)

Links

http://www.bumc.bu.edu/RenalSection

All recent recommendations

• 8.8
  Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis.
  Recommended by Kamyar Kalantar-Zadeh, Jurg Schifferli with Michael Mayr, Kenneth White with Emily G Farrow, Bradley Dixon, Csaba Kovesdy, Alan Yu with Jeanie Park, David Salant with Laurence H Beck Jr, Markus Ketteler
  
• 5.0
  VEGF inhibition and renal thrombotic microangiopathy.
  Recommended by Andrew Davenport, Terence H Cook with Candice Roufosse, David Salant with Ramon G Bonegio, Alejandro Chade
  
• 3.0
  Proteolytic processing of dynamin by cytoplasmic cathepsin L is a mechanism for proteinuric kidney disease.
  Recommended by David Salant with Dr Laurence Beck
  
• 4.8
  Loss of the tumor suppressor Vhlh leads to upregulation of Cxcr4 and rapidly progressive glomerulonephritis in mice.
  Recommended by Mauro Abbate, David Salant with Dr Ramon Bonegio
  
• 6.0
  Nck adaptor proteins link nephrin to the actin cytoskeleton of kidney podocytes.
  Recommended by David Salant with Dr Ramon Bonegio
  
• 6.0
  Nephrin ectodomain engagement results in Src kinase activation, nephrin phosphorylation, Nck recruitment, and actin polymerization.
  Recommended by David Salant with Dr Ramon Bonegio
  
• 3.0
  Hypoxia requires notch signaling to maintain the undifferentiated cell state.
  Recommended by David Salant with Ramon Bonegio
  
• 3.0
  Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy.
  Recommended by David Salant with Dr Laurence Beck
  
• 3.0
  Crosstalk between Jagged1 and GDNF/Ret/GFRalpha1 signalling regulates ureteric budding and branching.
  Recommended by David Salant with Dr Ramon Bonegio