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
    2018 FGF23 effects on the heart-levels, time, source, and context matter.Kidney International.  94:7-11. 2018
    2018 Fibroblast growth factor 23 and Klotho contribute to airway inflammation.European Respiratory Journal.  52. 2018
    2018 STAT3-enhancing germline mutations contribute to tumor-extrinsic immune evasion.Journal of Clinical Investigation.  128:1867-1872. 2018
    2018 FGF23 Actions on Target Tissues-With and Without Klotho.Frontiers in Endocrinology.  9:189. 2018
    2017 Klotho Inhibits Interleukin-8 Secretion from Cystic Fibrosis Airway Epithelia.Scientific Reports.  7:14388. 2017
    2017 Vitamin D treatment attenuates cardiac FGF23/FGFR4 signaling and hypertrophy in uremic rats.Nephrology Dialysis Transplantation.  32:1493-1503. 2017
    2017 Cardiac actions of fibroblast growth factor 23.BONE.  100:69-79. 2017
    2017 FGF23/FGFR4-mediated left ventricular hypertrophy is reversible.Scientific Reports.  7:1993. 2017
    2017 Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice.Journal of Visualized Experiments2017
    2017 Inflammation and elevated levels of fibroblast growth factor 23 are independent risk factors for death in chronic kidney disease.Kidney International.  91:711-719. 2017
    2017 Fibroblast Growth Factor 23: Mineral Metabolism and Beyond.Contributions to Nephrology.  190:83-95. 2017
    2016 Fibroblast growth factor 23 directly targets hepatocytes to promote inflammation in chronic kidney disease.Kidney International.  90:985-996. 2016
    2016 Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury.Journal of Clinical Investigation.  126:3336-3350. 2016
    2016 Induction of cardiac FGF23/FGFR4 expression is associated with left ventricular hypertrophy in patients with chronic kidney disease.Nephrology Dialysis Transplantation.  31:1088-1099. 2016
    2016 The Effect of a Gluten-Free Diet in Children With Difficult-to-Manage Nephrotic Syndrome.Pediatrics.  138. 2016
    2016 The role of fibroblast growth factor 23 and Klotho in uremic cardiomyopathy.Current Opinion in Nephrology and Hypertension.  25:314-324. 2016
    2015 Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.Cell Metabolism.  22:1020-1032. 2015
    2015 Hunt for the culprit of cardiovascular injury in kidney disease.Cardiovascular Research.  108:209-211. 2015
    2015 Klotho and phosphate are modulators of pathologic uremic cardiac remodeling.Journal of the American Society of Nephrology.  26:1290-1302. 2015
    2015 Sphingomyelinase-like phosphodiesterase 3b expression levels determine podocyte injury phenotypes in glomerular disease.Journal of the American Society of Nephrology.  26:133-147. 2015
    2014 Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD.Nephrology Dialysis Transplantation.  29:2028-2035. 2014
    2014 Paricalcitol downregulates myocardial renin-angiotensin and fibroblast growth factor expression and attenuates cardiac hypertrophy in uremic rats.American Journal of Hypertension.  27:720-726. 2014
    2014 Signal transduction in podocytes--spotlight on receptor tyrosine kinases.Nature Reviews Nephrology.  10:104-115. 2014
    2014 In vivo imaging of kidney glomeruli transplanted into the anterior chamber of the mouse eye.Scientific Reports.  4:3872. 2014
    2013 Transient receptor potential channel 6 (TRPC6) protects podocytes during complement-mediated glomerular disease.Journal of Biological Chemistry.  288:36598-36609. 2013
    2013 Abatacept in B7-1-positive proteinuric kidney disease.New England Journal of Medicine.  369:2416-2423. 2013
    2013 ARHGDIA mutations cause nephrotic syndrome via defective RHO GTPase signaling.Journal of Clinical Investigation.  123:3243-3253. 2013
    2013 Essential role for synaptopodin in dendritic spine plasticity of the developing hippocampus.Journal of Neuroscience.  33:12510-12518. 2013
    2013 Dynamin-mediated nephrin phosphorylation regulates glucose-stimulated insulin release in pancreatic beta cells (Journal of Biological Chemistry (2012) 287, (28932-28942))Journal of Biological Chemistry.  288:1277. 2013
    2012 Expression of fgf23 and αklotho in developing embryonic tissues and adult kidney of the zebrafish, Danio rerio.Nephrology Dialysis Transplantation.  27:4314-4322. 2012
    2012 The calcineurin-NFAT pathway allows for urokinase receptor-mediated beta3 integrin signaling to cause podocyte injury.The Clinical investigator.  90:1407-1420. 2012
    2012 Erratum to: The calcineurin-NFAT pathway allows for urokinase receptor-mediated beta3 integrin signaling to cause podocyte injuryThe Clinical investigator.  1. 2012
    2012 Dynamin-mediated Nephrin phosphorylation regulates glucose-stimulated insulin release in pancreatic beta cells.Journal of Biological Chemistry.  287:28932-28942. 2012
    2012 Regarding Maas's editorial letter on serum suPAR levels.Kidney International.  82:492. 2012
    2012 Fibroblast growth factor 23 and the heart.Current Opinion in Nephrology and Hypertension.  21:369-375. 2012
    2012 Rescue of tropomyosin deficiency in Drosophila and human cancer cells by synaptopodin reveals a role of tropomyosin α in RhoA stabilization.EMBO Journal.  31:1028-1040. 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)Journal of Clinical Investigation.  122:780. 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)Journal of Clinical Investigation.  122:781. 2012
    2011 Additional comments on response of Jiang et alProceedings of the Society for Experimental Biology and Medicine.  236:1363. 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 Ca21 and RhoA activation'.Proceedings of the Society for Experimental Biology and Medicine.  236:1361. 2011
    2011 FGF23 induces left ventricular hypertrophy.Journal of Clinical Investigation.  121:4393-4408. 2011
    2011 Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway.American Journal of Pathology.  179:1719-1732. 2011
    2011 CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival.Journal of Clinical Investigation.  121:3965-3980. 2011
    2011 Wnt/β-catenin pathway in podocytes integrates cell adhesion, differentiation, and survival.Journal of Biological Chemistry.  286:26003-26015. 2011
    2011 COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness.Journal of Clinical Investigation.  121:2013-2024. 2011
    2011 Mast cells, macrophages, and crown-like structures distinguish subcutaneous from visceral fat in mice.Journal of Lipid Research.  52:480-488. 2011
    2008 Mpv17l protects against mitochondrial oxidative stress and apoptosis by activation of Omi/HtrA2 protease.Proceedings of the National Academy of Sciences.  105:14106-14111. 2008
    2008 The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A.Nature Medicine.  14:931-938. 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.Molecular and Cellular Biology.  27:8215-8227. 2007
    2007 Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton.Trends in Cell Biology.  17:428-437. 2007
    2007 Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy.Nature Genetics.  39:1007-1012. 2007
    2007 Synaptopodin protects against proteinuria by disrupting Cdc42:IRSp53:Mena signaling complexes in kidney podocytes.American Journal of Pathology.  171:415-427. 2007
    2007 Nuclear relocation of the nephrin and CD2AP-binding protein dendrin promotes apoptosis of podocytes.Proceedings of the National Academy of Sciences.  104:10134-10139. 2007
    2006 Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signalling.Nature Cell Biology.  8:485-491. 2006
    2005 TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function.Nature Genetics.  37:739-744. 2005
    2005 Promotion of importin alpha-mediated nuclear import by the phosphorylation-dependent binding of cargo protein to 14-3-3.Journal of Cell Biology.  169:415-424. 2005
    2005 Synaptopodin regulates the actin-bundling activity of alpha-actinin in an isoform-specific manner.Journal of Clinical Investigation.  115:1188-1198. 2005
    2004 Induction of B7-1 in podocytes is associated with nephrotic syndrome.Journal of Clinical Investigation.  113:1390-1397. 2004
    2002 Novel concepts in understanding and management of glomerular proteinuria.Nephrology Dialysis Transplantation.  17:951-955. 2002
    2001 Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin.Journal of Clinical Investigation.  108:1621-1629. 2001
    2001 Differentiation- and stress-dependent nuclear cytoplasmic redistribution of myopodin, a novel actin-bundling proteinJournal of Cell Biology.  155:393-403. 2001
    2001 Differentiation- and stress-dependent nuclear cytoplasmic redistribution of myopodin, a novel actin-bundling protein.Journal of Cell Biology.  155:393-404. 2001
    Cardioprotective effects of paricalcitol alone and in combination with FGF23 receptor inhibition in chronic renal failure: experimental and clinical studiesAmerican Journal of Hypertension

    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

  • Doctor of Philosophy in Biological and Biomedical Sciences, Institution Not Available in List
  • Full Name

  • Christian Faul
  • Blazerid

  • cfaul