Ilse S Daehn, PhD Email Ilse Daehn
- ASSISTANT PROFESSOR | Medicine, Nephrology
Ilse Daehn has been an Assistant Professor in the Department of Medicine, Division of Nephrology, at the Icahn School of Medicine at Mount Sinai since 2013. Her research aims to understand chronic kidney disease development and progression. She is currently seeking biomarkers of disease progression at the Institute of Personalized Medicine.
Dr. Daehn holds a degree in Biotechnology (Honors) from Flinders University of South Australia. She performed a research placement at the Fundacion Jimenez Diaz, Madrid before starting her Doctorate studies at Flinders University of SA, and was awarded her PhD in 2007. She was a postdoctoral fellow at Cancer Research UK, in London and came to NYC to pursue a second postdoctoral fellowship at Mount Sinai.
Dr. Daehn is a member of DBRC and OAEM Steering Committees and former Co-chair of the Postdoc Executive Committee at Mount Sinai. She sits on NYC Tech Connect’s Entrepreneurial Scientist Advisory Panel.
Please visit her lab website at http://labs.icahn.mssm.edu/daehnlab/.
Cell Biology, Kidney, Mitochondria, Oxidative Stress
Bachelors, Flinders University
PhD, Flinders University
4D Award - Pilot Project Grant
National Center for Advancing Translational Science
Young Investigator Grant
National Kidney Foundation
Quod Erat Demonstrandum (QED) Special Recognition Award
Icahn School of Medicine at Mount Siani
My research focuses on exploring the complexity of signaling crosstalk between cells in the kidney. Particularly, my work aims to examine molecular mechanisms in the glomerulus that result in kidney disease progression and diabetic nephropathy in order to identify novel glomerular lesion-specific therapeutic targets and biomarkers. I have so far taken innovative approaches to examine the development of glomerular disease and the outcomes from this work have provided a fundamental paradigm shift in our current understanding of chronic kidney disease development.
Daehn I. Shift in Focus-To Explore the Role of the Endothelium in Kidney Disease. J Nephrol Renal Ther. 2016; 2(1): 004.
Atreya I, Diall A, Dvorsky R, Atreya R, Henninger C, Grün M, Hofmann U, Schaeffeler E, Lopez-Posadas R, Daehn I, Zenker S, Döbrönti M, Neufert C, Billmeier U, Zundler S, Fritz G, Schwab M, Neurath M. Designer Thiopurine-analogues for Optimised Immunosuppression in Inflammatory Bowel Diseases. J Crohns Colitis 2016 Oct; 10(10): 1132-1143.
Casalena G, Bottinger E, Daehn I. TGFβ-Induced Actin Cytoskeleton Rearrangement in Podocytes Is Associated with Compensatory Adaptation of Mitochondrial Energy Metabolism. Nephron 2015 Nov;.
Weins A, Wong JS, Basgen JM, Gupta R, Daehn I, Casagrande L, Lessman D, Schwartzman M, Meliambro K, Patrakka J, Shaw A, Tryggvason K, He JC, Nicholas SB, Mundel P, Campbell KN. Dendrin ablation prolongs life span by delaying kidney failure. The American journal of pathology 2015 Aug; 185(8).
Mallipattu SK, Horne SJ, D'Agati V, Narla G, Liu R, Frohman MA, Dickman K, Chen EY, Ma'ayan A, Bialkowska AB, Ghaleb AM, Nandan MO, Jain MK, Daehn I, Chuang PY, Yang VW, He JC. Krüppel-like factor 6 regulates mitochondrial function in the kidney. The Journal of clinical investigation 2015 Mar; 125(3).
Daehn I, Bottinger EP. Microvascular Endothelial Cells Poised to Take Center Stage in Experimental Renal Fibrosis. Journal of the American Society of Nephrology : JASN 2014 Dec;.
Casalena G, Krick S, Daehn I, Yu L, Ju W, Shi S, Tsai SY, D'Agati V, Lindenmeyer M, Cohen CD, Schlondorff D, Bottinger EP. Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro. American journal of physiology. Renal physiology 2014 Jun; 306(11).
Daehn I, Casalena G, Zhang T, Shi S, Fenninger F, Barasch N, Yu L, D'Agati V, Schlondorff D, Kriz W, Haraldsson B, Bottinger EP. Endothelial mitochondrial oxidative stress determines podocyte depletion in segmental glomerulosclerosis. The Journal of clinical investigation 2014 Apr; 124(4).
Gentle ME, Shi S, Daehn I, Zhang T, Qi H, Yu L, D'Agati VD, Schlondorff DO, Bottinger EP. Epithelial cell TGFβ signaling induces acute tubular injury and interstitial inflammation. Journal of the American Society of Nephrology : JASN 2013 Apr; 24(5).
Casalena G, Daehn I, Bottinger E. Transforming growth factor-β, bioenergetics, and mitochondria in renal disease. Seminars in nephrology 2012 May; 32(3).
Daehn I, Brem R, Barkauskaite E, Karran P. 6-Thioguanine damages mitochondrial DNA and causes mitochondrial dysfunction in human cells. FEBS letters 2011 Dec; 585(24).
Brem R, Daehn I, Karran P. Efficient DNA interstrand crosslinking by 6-thioguanine and UVA radiation. DNA repair 2011 Aug; 10(8).
Daehn IS, Varelias A, Rayner TE. T-lymphocyte-induced, Fas-mediated apoptosis is associated with early keratinocyte differentiation. Experimental dermatology 2010 Apr; 19(4).
Daehn I, Karran P. Immune effector cells produce lethal DNA damage in cells treated with a thiopurine. Cancer research 2009 Mar; 69(6).
Daehn IS, Varelias A, Rayner TE. Sodium butyrate induced keratinocyte apoptosis. Apoptosis : an international journal on programmed cell death 2006 Aug; 11(8).
Gangnuss S, Cowin AJ, Daehn IS, Hatzirodos N, Rothnagel JA, Varelias A, Rayner TE. Regulation of MAPK activation, AP-1 transcription factor expression and keratinocyte differentiation in wounded fetal skin. The Journal of investigative dermatology 2004 Mar; 122(3).
Blanco-Colio LM, Justo P, Daehn I, Lorz C, Ortiz A, Egido J. Bcl-xL overexpression protects from apoptosis induced by HMG-CoA reductase inhibitors in murine tubular cells. Kidney international 2003 Jul; 64(1).
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Dr.Daehn did not report having any of the following types of financial relationships with industry during 2018 and/or 2019: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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