• 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
    2022 Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in the Absence and Presence of Chronic Kidney DiseaseThe FASEB Journal.  36. 2022
    2022 Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signalingeLife.  11. 2022
    2022 The bone at the intersection of kidney and heart diseaseTrends in Pharmacological Sciences.  43:84-86. 2022
    2021 FGF23, a novel muscle biomarker detected in the early stages of ALSScientific Reports.  11. 2021
    2021 FGF21-FGFR4 signaling in cardiac myocytes promotes concentric cardiac hypertrophy in mouse models of diabetes 2021
    2021 Fibroblast growth factor 23 (FGF23) induces ventricular arrhythmias and prolongs QTc interval in mice in an FGF receptor 4-dependent manner 2021
    2021 DACH1 as a multifaceted and potentially druggable susceptibility factor for kidney diseaseJournal of Clinical Investigation.  131. 2021
    2020 Fibroblast Growth Factor Receptor 4 Deficiency Mediates Airway Inflammation in the Adult Healthy Lung?Frontiers in Medicine.  7. 2020
    2020 The Effects of the Anti-aging Protein Klotho on Mucociliary ClearanceFrontiers in Medicine.  6. 2020
    2019 FGFR4 does not contribute to progression of chronic kidney diseaseScientific Reports.  9. 2019
    2019 SMPDL3b modulates insulin receptor signaling in diabetic kidney diseaseNature Communications.  10. 2019
    2019 FGF23 and inflammation—a vicious coalition in CKDKidney International.  96:813-815. 2019
    2019 The role of fibroblast growth factor 23 in inflammation and anemiaInternational Journal of Molecular Sciences.  20. 2019
    2019 DNA-Encoded Library-Derived DDR1 Inhibitor Prevents Fibrosis and Renal Function Loss in a Genetic Mouse Model of Alport SyndromeACS Chemical Biology.  14:37-49. 2019
    2019 Cardioprotective Effects of Paricalcitol Alone and in Combination with FGF23 Receptor Inhibition in Chronic Renal Failure: Experimental and Clinical StudiesAmerican Journal of Hypertension.  32:34-44. 2019
    2019 Plasma zonulin levels in childhood nephrotic syndromeFrontiers in Pediatrics.  7. 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 matterKidney International.  94:7-11. 2018
    2018 Fibroblast growth factor 23 and Klotho contribute to airway inflammationEuropean Respiratory Journal.  52. 2018
    2018 FGF23 actions on target tissues-with and without KlothoFrontiers in Endocrinology.  9. 2018
    2018 STAT3-enhancing germline mutations contribute to tumor-extrinsic immune evasionJournal of Clinical Investigation.  128:1867-1872. 2018
    2017 FGF23/FGFR4-mediated left ventricular hypertrophy is reversibleScientific Reports.  7. 2017
    2017 Klotho Inhibits Interleukin-8 Secretion from Cystic Fibrosis Airway EpitheliaScientific Reports.  7. 2017
    2017 Vitamin D treatment attenuates cardiac FGF23/FGFR4 signaling and hypertrophy in uremic ratsNephrology Dialysis Transplantation.  32:1493-1503. 2017
    2017 Cardiac actions of fibroblast growth factor 23BONE.  100:69-79. 2017
    2017 Induction of an inflammatory response in primary hepatocyte cultures from miceJournal of Visualized Experiments.  2017. 2017
    2017 Inflammation and elevated levels of fibroblast growth factor 23 are independent risk factors for death in chronic kidney diseaseKidney International.  91:711-719. 2017
    2017 Fibroblast Growth Factor 23: Mineral Metabolism and beyondContributions to Nephrology.  190:83-95. 2017
    2016 Fibroblast growth factor 23 directly targets hepatocytes to promote inflammation in chronic kidney diseaseKidney International.  90:985-996. 2016
    2016 Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injuryJournal 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 diseaseNephrology Dialysis Transplantation.  31:1088-1099. 2016
    2016 The effect of a gluten-free diet in children with difficult-to-manage nephrotic syndromePediatrics.  138. 2016
    2016 The role of fibroblast growth factor 23 and Klotho in uremic cardiomyopathyCurrent Opinion in Nephrology and Hypertension.  25:314-324. 2016
    2015 Klotho and phosphate are modulators of pathologic uremic cardiac remodelingJournal of the American Society of Nephrology.  26:1290-1302. 2015
    2015 Hunt for the culprit of cardiovascular injury in kidney diseaseCardiovascular Research.  108:209-211. 2015
    2015 Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular HypertrophyCell Metabolism.  22:1020-1032. 2015
    2015 Sphingomyelinase-like phosphodiesterase 3b expression levels determine podocyte injury phenotypes in glomerular diseaseJournal 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 CKDNephrology Dialysis Transplantation.  29:2028-2035. 2014
    2014 Paricalcitol downregulates myocardial renin-angiotensin and fibroblast growth factor expression and attenuates cardiac hypertrophy in uremic ratsAmerican Journal of Hypertension.  27:720-726. 2014
    2014 Signal transduction in podocytes - Spotlight on receptor tyrosine kinasesNature Reviews Nephrology.  10:104-115. 2014
    2014 In vivo imaging of kidney glomeruli transplanted into the anterior chamber of the mouse eyeScientific Reports.  4. 2014
    2013 Transient receptor potential channel 6 (trpc6) protects podocytes during complement-Mediated glomerular diseaseJournal of Biological Chemistry.  288:36598-36609. 2013
    2013 ARHGDIA mutations cause nephrotic syndrome via defective RHO GTPase signalingJournal of Clinical Investigation.  123:3243-3253. 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))Journal of Biological Chemistry.  288:1277. 2013
    2013 Abatacept in B7-1-positive proteinuric kidney diseaseNew England Journal of Medicine.  369:2416-2423. 2013
    2012 Expression of fgf23 and αklotho in developing embryonic tissues and adult kidney of the zebrafish, Danio rerioNephrology Dialysis Transplantation.  27:4314-4322. 2012
    2012 Dynamin-mediated nephrin phosphorylation regulates glucose-stimulated insulin release in pancreatic beta cellsJournal of Biological Chemistry.  287:28932-28942. 2012
    2012 Regarding Maas's editorial letter on serum suPAR levelsKidney International.  82:492. 2012
    2012 Fibroblast growth factor 23 and the heartCurrent 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 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
    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 hypertrophyJournal of Clinical Investigation.  121:4393-4408. 2011
    2011 CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survivalJournal of Clinical Investigation.  121:3965-3980. 2011
    2011 Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathwayAmerican Journal of Pathology.  179:1719-1732. 2011
    2011 Wnt/β-catenin pathway in podocytes integrates cell adhesion, differentiation, and survivalJournal of Biological Chemistry.  286:26003-26015. 2011
    2011 COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafnessJournal of Clinical Investigation.  121:2013-2024. 2011
    2011 Mast cells, macrophages, and crown-like structures distinguish subcutaneous from visceral fat in miceJournal of Lipid Research.  52:480-488. 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 ANature 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 myocytesMolecular and Cellular Biology.  27:8215-8227. 2007
    2007 Actin up: regulation of podocyte structure and function by components of the actin cytoskeletonTrends in Cell Biology.  17:428-437. 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 cardiomyopathyNature Genetics.  39:1007-1012. 2007
    2007 Synaptopodin protects against proteinuria by disrupting Cdc42:IRSp53:Mena signaling complexes in kidney podocytesAmerican Journal of Pathology.  171:415-427. 2007
    2006 Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signallingNature Cell Biology.  8:485-491. 2006
    2005 TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal functionNature Genetics.  37:739-744. 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 mannerJournal of Clinical Investigation.  115:1188-1198. 2005
    2004 Induction of B7-1 in podocytes is associated with nephrotic syndromeJournal of Clinical Investigation.  113:1390-1397. 2004
    2002 Novel concepts in understanding and management of glomerular proteinuriaNephrology Dialysis Transplantation.  17:951-955. 2002
    2001 Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrinJournal of Clinical Investigation.  108:1621-1629. 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


    Year Title Altmetric
    2021 Fibroblast Growth Factor 23 2021
    2021 Introduction 2021


    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.
  • Principal Investigator On

  • Activation of Cardiac FGFR4 Causes Left Ventricular Hypertrophy  awarded by National Heart, Lung, and Blood Institute/NIH/DHHS
  • Changes in Phosphate Metabolism cause Pathologic Cardiac Remodeling in Chronic Kidney Disease (CKD)  awarded by Indiana University
  • FGF21 Causes Left Ventricular Hypertrophy  awarded by American Diabetes Association, Inc.
  • FGF23 Contributes To Anemia In Chronic Kidney Disease By Elevating Hepcidin Production  awarded by National Institute of Diabetes and Digestive and Kidney Diseases/NIH/DHHS
  • Hyperphosphatemia Contributes to Cardiac Injury in Chronic Kidney Disease  awarded by National Institute of Diabetes and Digestive and Kidney Diseases/NIH/DHHS
  • Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in the Absence and Presence of Chronic Kidney Disease  awarded by National Institute of Diabetes and Digestive and Kidney Diseases/NIH/DHHS
  • Hyperphosphatemia Contributes to Systemic Inflammation and Anemia in Chronic Kidney Disease  awarded by National Institute of Diabetes and Digestive and Kidney Diseases/NIH/DHHS
  • Paracrine Actions of Fibroblasts Promote Pathologic Cardiac Myocyte Remodeling in Duchenne Muscular Dystrophy  awarded by Indiana University
  • Private Grant  awarded by Bayer AG
  • Private Grant  awarded by AMGEN, INC.^
  • Targeting sKlotho-FGF23 Interactions to Improve Pathological Phosphate Handling in CKD  awarded by Indiana University
  • Vitamin D and Soluble Klotho Inhibit FGF23-Mediated Cardiac Hypertrophy in Chronic Kidney Disease  awarded by National Institute of Diabetes and Digestive and Kidney Diseases/NIH/DHHS
  • 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
  • Doctor of Philosophy in Biological and Biomedical Sciences, 2005
  • Full Name

  • Christian Faul