New Faculty

Dr. Steven Funk joins the Department of Medicine

Dr. Steven Funk joined the Department of Medicine in the Division of Nephrology as an Instructor in November, 2019.

Dr. Funk’s major interest is the regulation of cellular functions by cell-matrix and cell-cell adhesion, with a focus on how renal glomerular basement membrane (GBM) defects in the kidney affect the podocyte cells that attach to the GBM and mediate filtration. During his thesis work in Dr. Wayne Orr’s laboratory, he investigated how extracellular matrices deferentially influence endothelial cell quiescence and inflammation through integrin-mediated signaling pathways in the context of shear stress. Additionally, he elucidated that the pro-inflammatory signaling and gene expression downstream of the cell-cell receptor EphA2 in endothelial cells in response to atherosclerosis-associated stimuli are mediated by the nuclear factor of activated T cells (NFAT) transcription factor.

Dr. Funk joined Jeff Miner’s laboratory for post-doctoral studies with the aims to gain expertise in animal modeling and to continue investigating how extracellular matrix impacts cell function by studying the kidney’s glomerular basement membrane and the cells attached to it that mediate filtration of the blood, called podocytes. In Dr. Miner’s lab, he characterized the first example of a glomerular basement membrane matrix mutation (human lamininβ2-S80R) that can exacerbate Alport syndrome, a major monogenic disease that exhibits high phenotypic variability, revealing new insight into both glomerular filtration and Alport syndrome variability. Additionally he has shown that conditional endothelial cell expression of a gene (collagen IV alpha 3) that is lost in Alport syndrome cannot replace podocyte expression of this gene, thereby defining potential gene therapy approaches. His continuing work is focused on mechanisms of lamininβ2 in filtration through a new polymerization-defective lamininβ2 mutation, the effects of albumin on nephron epithelium in nephrotic states of Alport and Pierson syndrome contexts, and the effects of the intermediate filament desmin on podocyte pathology.