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Faculty Detail    
Name CHRISTIAN FAUL
  
Campus Address THT 611L Zip 0007
Phone  (205) 996-9641
E-mail  cfaul@uabmc.edu
Other websites
     

Education
Undergraduate  Ruprecht Karls University Heidelberg, Germany    1999  Diploma in Biology 
Graduate  Albert Einstein College of Medicine, Bronx, NY    2005  PhD 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Med - Nephrology  Med - Nephrology Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Comprehensive Cardiovascular Ctr  Comprehensive Cardiovascular Ctr Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Professor
Center  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Professor
Center  Integrative Center for Aging Research  Integrative Center for Aging Research Professor
Center  Nephrology Research & Training Center  Nephrology Research & Training Center Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 

Biographical Sketch 
Dr. Christian Faul received his undergraduate training in cell and molecular biology at the Ruprecht Karls University Heidelberg in Germany from 1993-1999. He earned his PhD title at the Albert Einstein College of Medicine in the Bronx in 2005, and he conducted his postdoctoral research training at the Mount Sinai School of Medicine in New York City. In 2008, Dr. Faul became a faculty member in the Department of Medicine and in the Department of Cell Biology & Anatomy at the University of Miami Leonard M. Miller School of Medicine. In 2017, he joined the University of Alabama at Birmingham where he currently holds the rank of Associate Professor in the Division of Nephrology within the Department of Medicine and in the Department of Cell, Developmental and Integrative Biology (CDIB). He is also a member of the Section of Cardio-Renal Physiology and Medicine and the Comprehensive Diabetes Center. Dr. Faul is a cell biologist who has a strong interest in translational medicine, especially in pathomechanisms underlying diseases of the kidney and the heart. He has formed a versatile team of collaborators, ranging from basic to clinical scientists, nephrologists to cardiologist, physiologists to geneticists. Dr. Faul’s laboratory studies signal transduction pathways in cardiac myocytes that regulate cardiac remodeling with the goal to identify novel drug targets for cardiac hypertrophy and heart failure. He focuses on circulating fibroblast growth factors and their pathological effects on the heart in the context of chronic kidney disease and diabetes. In collaborations with pharma industry, Dr. Faul analyzes beneficial cardiac effects of pharmacological blockers for fibroblast growth factor receptors in animal models with kidney injury and diabetes. Dr. Faul received research funding from the American Heart Association (AHA), the American Diabetes Association (ADA), the American Society of Nephrology (ASN), and the NephCure Foundation, as well as support from pharma industry. In summer of 2015, he received an R01 grant from the NIH/NHLBI. Dr. Faul is extremely dedicated to the training of graduate students and postdoctoral research fellows, and his laboratory provides a diverse environment in which cell biological, cardiovascular and renal researchers can be trained. Four of his graduate students have received NRSA fellowships from the NIH, and his PostDocs have received fellowships from international funding organizations, such as the AHA, as well as support from industry.

Society Memberships
Organization Name Position Held Org Link
American Diabetes Association     
American Heart Association     
American Society of Nephrology     
 



Research/Clinical Interest
Title
The role of endocrine Fibroblast Growth Factors in Chronic Kidney Disease and Diabetes and in associated pathologies.
Description
The overall goal of my laboratory is to study molecular mechanisms that regulate the function of renal podocytes as well as cardiac myocytes. We employ a variety of different biochemical and cell biological techniques in order to study signal transduction in vitro and we use different genetic mouse models to validate our findings in vivo. By analyzing signaling pathways that regulate the actin cytoskeleton and gene expression in podocytes, we wish to characterize molecular events that are involved in the development of proteinuric kidney diseases. In cardiac myocytes, we focus on signaling pathways that induce cardiac remodeling and contribute to heart failure. In the past 8 years, we have extended our research interest to combining the analysis of pathological signaling events in kidney and heart. We study cardiac hypertrophy and fibrosis in the context of chronic kidney disease (CKD) - also called uremic cardiomyopathy - with the focus on the characterization of novel circulating mediators. My laboratory has identified for the first time direct cardiac effects of fibroblast growth factor (FGF) 23 in animal models of CKD, including the underlying signaling pathway (Faul C et al., The Journal of Clinical Investigation 2011). More recently, we have identified FGF receptor (FGFR) 4 as the mediator of pathological FGF23 effects in the heart (Grabner A et al., Cell Metabolism 2015). Our ongoing research focuses on a more detailed analysis of cardiac FGF23/FGFR4 signaling in different animal models of primary and secondary cardiac injury. Furthermore, we determine if FGF23 can target and potentially harm other tissues via FGFR4. Our recent findings indicate that FGF23 can activate FGFR4 on hepatocytes thereby inducing expression and secretion of inflammatory cytokines and potentially contributing to systemic inflammation associated with chronic kidney disease (Singh S et al., Kidney International 2016). In parallel to our work on FGF23, we have recently initiated studies which focus on FGF21, another member of the family of endocrine FGFs. We determine whether FGF21 can directly target the heart, via similar mechanisms as FGF23, and thereby contribute to cardiac injury in the context of diabetes (also called diabetic cardiomyopathy). Ongoing projects include: • Analyzing the regulation of FGFR4 signaling in cultured cardiac myocytes and hepatocytes. • Characterizing the effects of FGF23/FGFR4 activation in the heart in different animal models of primary and secondary cardiac injury. • Determining the role of FGF23/FGFR4 signaling in the liver, with focus on inflammation and iron metabolism. • Analyzing the effects of FGF21/FGFR4 signaling in the heart. • Studying beneficial effects of pharmacologic FGFR4 blockade in animal models of chronic kidney disease and diabetes.

Selected Publications 
Publication PUBMEDID
Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.
Grabner A, Amaral AP, Schramm K, Singh S, Sloan A, Yanucil C, Li J, Shehadeh LA, Hare JM, David V, Martin A, Fornoni A, Di Marco GS, Kentrup D, Reuter S, Mayer AB, Pavenstädt H, Stypmann J, Kuhn C, Hille S, Frey N, Leifheit-Nestler M, Richter B, Haffner D, Abraham R, Bange J, Sperl B, Ullrich A, Brand M, Wolf M, Faul C.
Cell Metab. 2015 Dec 1;22(6):1020-32. 		 26437603 
FGF23/FGFR4-mediated left ventricular hypertrophy is reversible.
Grabner A, Schramm K, Silswal N, Hendrix M, Yanucil C, Czaya B, Singh S, Wolf M, Hermann S, Stypmann J, Di Marco GS, Brand M, Wacker MJ, Faul C.
Sci Rep. 2017 May 16;7(1):1993. 		 28512310 
FGF23 induces left ventricular hypertrophy.
Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, Gutiérrez OM, Aguillon-Prada R, Lincoln J, Hare JM, Mundel P, Morales A, Scialla J, Fischer M, Soliman EZ, Chen J, Go AS, Rosas SE, Nessel L, Townsend RR, Feldman HI, St John Sutton M, Ojo A, Gadegbeku C, Di Marco GS, Reuter S, Kentrup D, Tiemann K, Brand M, Hill JA, Moe OW, Kuro-O M, Kusek JW, Keane MG, Wolf M.
J Clin Invest. 2011 Nov;121(11):4393-408. 		 21985788 
Fibroblast growth factor 23 directly targets hepatocytes to promote inflammation in chronic kidney disease.
Singh S, Grabner A, Yanucil C, Schramm K, Czaya B, Krick S, Czaja MJ, Bartz R, Abraham R, Di Marco GS, Brand M, Wolf M, Faul C.
Kidney Int. 2016 Nov;90(5):985-996. 		 27457912 
Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice.
Czaya B, Singh S, Yanucil C, Schramm K, Faul C, Grabner A.
J Vis Exp. 2017 Mar 10;(121). 		 28362385 
The role of fibroblast growth factor 23 and Klotho in uremic cardiomyopathy.
Grabner A, Faul C.
Curr Opin Nephrol Hypertens. 2016 Jul;25(4):314-24. 		 27219043 
Cardiac actions of fibroblast growth factor 23.
Faul C.
Bone. 2017 Jul;100:69-79. 		 27725315 
Fibroblast Growth Factor 23: Mineral Metabolism and Beyond.
Grabner A, Mazzaferro S, Cianciolo G, Krick S, Capelli I, Rotondi S, Ronco C, La Manna G, Faul C.
Contrib Nephrol. 2017;190:83-95. 		 28535521 
Signal transduction in podocytes--spotlight on receptor tyrosine kinases.
Reiser J, Sever S, Faul C.
Nat Rev Nephrol. 2014 Feb;10(2):104-15. 		 24394191 
Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton.
Faul C, Asanuma K, Yanagida-Asanuma E, Kim K, Mundel P.
Trends Cell Biol. 2007 Sep;17(9):428-37. 		 17804239 
The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A.
Faul C, Donnelly M, Merscher-Gomez S, Chang YH, Franz S, Delfgaauw J, Chang JM, Choi HY, Campbell KN, Kim K, Reiser J, Mundel P.
Nat Med. 2008 Sep;14(9):931-8. 		 18724379 
Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway.
Nijenhuis T, Sloan AJ, Hoenderop JG, Flesche J, van Goor H, Kistler AD, Bakker M, Bindels RJ, de Boer RA, Möller CC, Hamming I, Navis G, Wetzels JF, Berden JH, Reiser J, Faul C, van der Vlag J.
Am J Pathol. 2011 Oct;179(4):1719-32. 		 21839714 
COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness.
Heeringa SF, Chernin G, Chaki M, Zhou W, Sloan AJ, Ji Z, Xie LX, Salviati L, Hurd TW, Vega-Warner V, Killen PD, Raphael Y, Ashraf S, Ovunc B, Schoeb DS, McLaughlin HM, Airik R, Vlangos CN, Gbadegesin R, Hinkes B, Saisawat P, Trevisson E, Doimo M, Casarin A, Pertegato V, Giorgi G, Prokisch H, Rötig A, Nürnberg G, Becker C, Wang S, Ozaltin F, Topaloglu R, Bakkaloglu A, Bakkaloglu SA, Müller D, Beissert A, Mir S, Berdeli A, Varpizen S, Zenker M, Matejas V, Santos-Ocaña C, Navas P, Kusakabe T, Kispert A, Akman S, Soliman NA, Krick S, Mundel P, Reiser J, Nürnberg P, Clarke CF, Wiggins RC, Faul C, Hildebrandt F.
J Clin Invest. 2011 May;121(5):2013-24. 		 21540551 
The Effect of a Gluten-Free Diet in Children With Difficult-to-Manage Nephrotic Syndrome.
Lemley KV, Faul C, Schramm K, Meyers K, Kaskel F, Dell KM, Gipson DS, Gibson K, Trachtman H.
Pediatrics. 2016 Jul;138(1). pii: e20154528. 		 27338701 
Protein kinase A, Ca2+/calmodulin-dependent kinase II, and calcineurin regulate the intracellular trafficking of myopodin between the Z-disc and the nucleus of cardiac myocytes.
Faul C, Dhume A, Schecter AD, Mundel P.
Mol Cell Biol. 2007 Dec;27(23):8215-27. 		 17923693 
Promotion of importin alpha-mediated nuclear import by the phosphorylation-dependent binding of cargo protein to 14-3-3.
Faul C, Hüttelmaier S, Oh J, Hachet V, Singer RH, Mundel P.
J Cell Biol. 2005 May 9;169(3):415-24. 		 15883195 
 

Keywords
chronic kidney disease, uremic cardiomyopathy, diabetic cardiomyopathy, FGF23, FGF21, Klotho, signal transduction