Positions

Overview

  • 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 his first 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. Five 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 and the DFG from Germany, as well as support from industry.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2019 SMPDL3b modulates insulin receptor signaling in diabetic kidney disease 2019
    2019 FGF23 and inflammation—a vicious coalition in CKD 2019
    2019 The Role of Fibroblast Growth Factor 23 in Inflammation and Anemia 2019
    2019 DNA-Encoded Library-Derived DDR1 Inhibitor Prevents Fibrosis and Renal Function Loss in a Genetic Mouse Model of Alport Syndrome 2019
    2019 Cardioprotective Effects of Paricalcitol Alone and in Combination with FGF23 Receptor Inhibition in Chronic Renal Failure: Experimental and Clinical Studies 2019
    2019 Plasma zonulin levels in childhood nephrotic syndrome 2019
    2019 Role of fibroblast growth factor 23 and klotho cross talk in idiopathic pulmonary fibrosis 2019
    2018 FGF23 effects on the heart—levels, time, source, and context matter 2018
    2018 Fibroblast growth factor 23 and Klotho contribute to airway inflammation 2018
    2018 FGF23 actions on target tissues-with and without Klotho 2018
    2018 STAT3-enhancing germline mutations contribute to tumor-extrinsic immune evasion 2018
    2017 FGF23/FGFR4-mediated left ventricular hypertrophy is reversible 2017
    2017 Klotho Inhibits Interleukin-8 Secretion from Cystic Fibrosis Airway Epithelia 2017
    2017 Cardiac actions of fibroblast growth factor 23 2017
    2017 Induction of an inflammatory response in primary hepatocyte cultures from mice 2017
    2017 Inflammation and elevated levels of fibroblast growth factor 23 are independent risk factors for death in chronic kidney disease 2017
    2017 Fibroblast Growth Factor 23: Mineral Metabolism and beyond 2017
    2017 Vitamin D treatment attenuates cardiac FGF23/FGFR4 signaling and hypertrophy in uremic rats 2017
    2016 Fibroblast growth factor 23 directly targets hepatocytes to promote inflammation in chronic kidney disease 2016
    2016 Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury 2016
    2016 The effect of a gluten-free diet in children with difficult-to-manage nephrotic syndrome 2016
    2016 The role of fibroblast growth factor 23 and Klotho in uremic cardiomyopathy 2016
    2016 Induction of cardiac FGF23/FGFR4 expression is associated with left ventricular hypertrophy in patients with chronic kidney disease 2016
    2015 Klotho and phosphate are modulators of pathologic uremic cardiac remodeling 2015
    2015 Hunt for the culprit of cardiovascular injury in kidney disease 2015
    2015 Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy 2015
    2015 Sphingomyelinase-like phosphodiesterase 3b expression levels determine podocyte injury phenotypes in glomerular disease 2015
    2014 Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD 2014
    2014 Signal transduction in podocytes - Spotlight on receptor tyrosine kinases 2014
    2014 In vivo imaging of kidney glomeruli transplanted into the anterior chamber of the mouse eye 2014
    2014 Paricalcitol downregulates myocardial renin-angiotensin and fibroblast growth factor expression and attenuates cardiac hypertrophy in uremic rats 2014
    2013 Transient receptor potential channel 6 (trpc6) protects podocytes during complement-Mediated glomerular disease 2013
    2013 ARHGDIA mutations cause nephrotic syndrome via defective RHO GTPase signaling 2013
    2013 Essential role for synaptopodin in dendritic spine plasticity of the developing hippocampus 2013
    2013 Dynamin-mediated nephrin phosphorylation regulates glucose-stimulated insulin release in pancreatic beta cells (Journal of Biological Chemistry (2012) 287, (28932-28942)) 2013
    2013 Abatacept in B7-1-positive proteinuric kidney disease 2013
    2012 Expression of fgf23 and αklotho in developing embryonic tissues and adult kidney of the zebrafish, Danio rerio 2012
    2012 Erratum to: The calcineurin-NFAT pathway allows for urokinase receptor-mediated beta3 integrin signaling to cause podocyte injury 2012
    2012 Dynamin-mediated nephrin phosphorylation regulates glucose-stimulated insulin release in pancreatic beta cells 2012
    2012 Regarding Maas's editorial letter on serum suPAR levels. 2012
    2012 Fibroblast growth factor 23 and the heart 2012
    2012 Rescue of tropomyosin deficiency in Drosophila and human cancer cells by synaptopodin reveals a role of tropomyosin α in RhoA stabilization 2012
    2012 Erratum: CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival (The Journal of Clinical Investigation (2011) 121, 10, (3965-3980) DOI: 10.1172/JCI58552) 2012
    2012 Erratum: Synaptopodin regulates the actin-bundling activity of a-actinin in an isoform-specific manner (Journal of Clinical Investigation (2005) 115, 5, (1188-1198) DOI: 10.1172/JCI23371) 2012
    2012 The calcineurin-NFAT pathway allows for urokinase receptor-mediated beta3 integrin signaling to cause podocyte injury 2012
    2011 Additional comments on response of Jiang et al 2011
    2011 TRPC6 in podocytes: Questions and commentary on the article by Jiang et al., 'Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskeleton rearrangement through increases of intracellular Ca 2+ and RhoA activation' 2011
    2011 FGF23 induces left ventricular hypertrophy 2011
    2011 CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival 2011
    2011 Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway 2011
    2011 Wnt/β-catenin pathway in podocytes integrates cell adhesion, differentiation, and survival 2011
    2011 COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness 2011
    2011 Mast cells, macrophages, and crown-like structures distinguish subcutaneous from visceral fat in mice 2011
    2008 Mpv17l protects against mitochondrial oxidative stress and apoptosis by activation of Omi/HtrA2 protease 2008
    2008 The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A 2008
    2007 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 2007
    2007 Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton 2007
    2007 Nuclear relocation of the nephrin and CD2AP-binding protein dendrin promotes apoptosis of podocytes 2007
    2007 Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy 2007
    2007 Synaptopodin protects against proteinuria by disrupting Cdc42:IRSp53:Mena signaling complexes in kidney podocytes 2007
    2006 Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signalling 2006
    2005 TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function 2005
    2005 Promotion of importin α-mediated nuclear import by the phosphorylation-dependent binding of cargo protein to 14-3-3 2005
    2005 Synaptopodin regulates the actin-bundling activity of α-actinin in an isoform-specific manner 2005
    2004 Induction of B7-1 in podocytes is associated with nephrotic syndrome 2004
    2002 Novel concepts in understanding and management of glomerular proteinuria 2002
    2001 Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin 2001
    2001 Differentiation- and stress-dependent nuclear cytoplasmic redistribution of myopodin, a novel actin-bundling protein 2001
    2001 Differentiation- and stress-dependent nuclear cytoplasmic redistribution of myopodin, a novel actin-bundling protein 2001

    Chapter

    Year Title Altmetric
    2014 The podocyte cytoskeleton: Key to a functioning glomerulus in health and disease.  22-53. 2014

    Research Overview

  • 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).

    • 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.
  • Teaching Overview

  • Graduate Biomedical Sciences (GBS) Program at UAB
    • Basic Biological Organization (GBS 709): “Receptor-mediated signaling” - core curriculum lecture series
    • Advanced Study of Renal Physiology (GBSC 732) - lecture series
    • Cardio-Renal Physiology (GBSC 700) - journal club
  • Education And Training

  • Mount Sinai School of Medicine Medicine - Nephrology, Postdoctoral Fellowship 2008
  • Full Name

  • Christian Faul