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Experimental models of immunological glomerular diseases and autoimmunity resembling those seen in man are used to obtain a fundamental understanding of the immunopathogenetic mechanisms of injury.
Antibody-mediated podocyte injury:
The primary focus of the Salant laboratory 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 and morphology of glomerular visceral epithelial cells (podocytes).
1. We have identified the target antigen in human membranous nephropathy as the phospholipase A2 receptor (PLA2R) and shown that about 75% of patients have circulating ant-PLA2R autoantibodies. Current work is directed at defining the mechanisms of podocyte injury induced by anti-PLA2R using a combination of in vitro, in vivo and human genetic techniques. Additional studies will explore the role of anti-PLA2R in the development of recurrent membranous nephropathy post renal transplantation.
2. Ongoing interests include the role of podocyte-specific antibodies, and the effects of complement-mediated injury on podocyte structure, composition of the filtration slit diaphragm and its attachment to the cytoskeleton, and on cell-matrix adhesion using animal models, cell biological and immunochemical methodologies.
Experimental models of immunological glomerular diseases and autoimmunity resembling those seen in man are used to obtain a fundamental understanding of the immunopathogenetic mechanisms of injury.
Antibody-mediated podocyte injury:
The primary focus of the Salant laboratory 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 and morphology of glomerular visceral epithelial cells (podocytes).
1. We have identified the target antigen in human membranous nephropathy as the phospholipase A2 receptor (PLA2R) and shown that about 75% of patients have circulating ant-PLA2R autoantibodies. Current work is directed at defining the mechanisms of podocyte injury induced by anti-PLA2R using a combination of in vitro, in vivo and human genetic techniques. Additional studies will explore the role of anti-PLA2R in the development of recurrent membranous nephropathy post renal transplantation.
2. Ongoing interests include the role of podocyte-specific antibodies, and the effects of complement-mediated injury on podocyte structure, composition of the filtration slit diaphragm and its attachment to the cytoskeleton, and on cell-matrix adhesion using animal models, cell biological and immunochemical methodologies.
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Fei Liu,Sarah T Ryan,Kelly C Fahnoe,Jennifer G Morgan, Anne E Cheung,Michael J Storek, Alejandro Best,Hui A Chen,Monica Locatelli, Shuyun Xu,Enno Schmidt,Leon F Schmidt-Jiménez,
Molecular therapy : the journal of the American Society of Gene Therapyno. 4 (2024): 1061-1079
Journal of the American Society of Nephrology : JASNno. 5 (2023): 737-750
Sudhir Kumar,Xueping Fan, Emily Zaltz, Hui Chen,Joel M. Henderson,David J. Salant,Hongying Yang,Stephen Berasi,Weining Lu
Journal of the American Society of Nephrologyno. 11S (2022): 513-513
F. Liu, S. Ryan, K. Fahnoe, J. Morgan,K. Bieber, E. Schmidt,A. Verschoor,R.J. Ludwig,D.J. Salant,J.M. Thurman,V.M. Holers,S. Violette,
Yogesh Gowthaman, Yiqing Guo,Jesse A. Pace,Robert Bronstein,John C. He,David J. Salant,Sandeep K. Mallipattu
Journal of the American Society of Nephrologyno. 11S (2022): 40-40
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