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.
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.
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