Professor Schneider was recruited in September 2007 as the incoming Head of Cardiovascular Science for the National Heart and Lung Institute, and served as Head of NHLI from 1 January 2009 through 31 August 2011.
He was educated at Harvard, the University of Pennsylvania, and Duke, followed by research training at the NIH under Nobel Laureate Marshall Nirenberg. In 1984, he was appointed to the nascent program in cardiac molecular biology at Baylor College of Medicine, ultimately becoming Professor of Medicine, Molecular & Cellular Biology, and Molecular Physiology & Biophysics, Director of the Center for Cardiovascular Development, and inaugural recipient of the M. D. Anderson Foundation Chair. His trainees number more than 80, and have been recognized by young investigator competitions and professorships world-wide.
Professor Schneider is the British Heart Foundation Simon Marks Professor of Regenerative Cardiology and Director of Imperial's BHF Centre for Research Excellence (2008-2019). He is the recipient of a Royal Society Wolfson Research Merit Award, an ERC Advanced Investigator Grant, the 2007 Distinguished Achievement Award of the American Heart Association Council on Basic Cardiovascular Sciences, the 2008 Medical Futures Cardiovascular Innovation Award, the 2010 Duke Medical Alumni Award, the 2011 Annual Clinical School Lecture at Cambridge, the 2011 Mikamo Lectureship of the Japanese Circulation Society, and the 2012 Jeffrey Isner Memorial Lecture at Tufts University.
He currently serves on peer-review panels for the Wellcome Trust and ERC, is a Governor of the Royal Brompton and Harefield NHS Foundation Trust, and serves as a member of the MRC Council (2008-2016).
Professor Schneider heads the Cardiac Myogenesis, Death and Regeneration research group.
Read his 2012 profile in Circulation:
et al., 2015, Forward Programming of Cardiac Stem Cells by Homogeneous Transduction with MYOCD plus TBX5, PLOS One, Vol:10, ISSN:1932-6203
et al., 2015, PDGFR alpha demarcates the cardiogenic clonogenic Sca1(+) stem/progenitor cell in adult murine myocardium, Nature Communications, Vol:6, ISSN:2041-1723
Dimmeler S, Zeiher AM, Schneider MD, 2005, Unchain my heart: the scientific foundations of cardiac repair., Journal of Clinical Investigation, Vol:115, ISSN:0021-9738, Pages:572-583
et al., 2005, Overlapping roles of pocket proteins in the myocardium are unmasked by germ line deletion of p130 plus heart-specific deletion of Rb., Molecular and Cellular Biology, Vol:25, ISSN:0270-7306, Pages:2486-2497
et al., 2014, HGK/MAP4K4 deficiency induces TRAF2 stabilization and Th17 differentiation leading to insulin resistance, Nature Communications, Vol:5, ISSN:2041-1723
et al., 2014, Hhex and Cer1 Mediate the Sox17 Pathway for Cardiac Mesoderm Formation in Embryonic Stem Cells, Stem Cells, Vol:32, ISSN:1066-5099, Pages:1515-1526
et al., 2014, T-1 Mapping Detects Pharmacological Retardation of Diffuse Cardiac Fibrosis in Mouse Pressure-Overload Hypertrophy, Circulation-Cardiovascular Imaging, Vol:7, ISSN:1941-9651, Pages:240-249
Mercola M, Ruiz-Lozano P, Schneider MD, 2011, Cardiac muscle regeneration: lessons from development, Genes & Development, Vol:25, ISSN:0890-9369, Pages:299-309
et al., 2010, Endogenous retinoic acid regulates cardiac progenitor differentiation, Proceedings of the National Academy of Sciences of the United States of America, Vol:107, ISSN:0027-8424, Pages:9234-9239
et al., 2007, Sox17 is essential for the specification of cardiac mesoderm in embryonic stem cells., Proceedings of the National Academy of Sciences of the United States of America, Vol:104, ISSN:0027-8424, Pages:3859-3864
et al., 2007, Ménage-à-trois 1 is critical for the transcriptional function of PPARgamma coactivator 1., Cell Metabolism, Vol:5, ISSN:1550-4131, Pages:129-142
et al., 2006, A pivotal role for endogenous TGF-beta-activated kinase-1 in the LKB1/AMP-activated protein kinase energy-sensor pathway., Proceedings of the National Academy of Sciences of the United States of America, Vol:103, ISSN:0027-8424, Pages:17378-17383
et al., 2004, Activation of cardiac Cdk9 represses PGC-1 and confers a predisposition to heart failure., EMBO Journal, Vol:23, ISSN:0261-4189, Pages:3559-3569
et al., 2003, Cardiac progenitor cells from adult myocardium: homing, differentiation, and fusion after infarction., Proceedings of the National Academy of Sciences of the United States of America, Vol:100, ISSN:0027-8424, Pages:12313-12318
et al., 2003, A Wnt- and beta -catenin-dependent pathway for mammalian cardiac myogenesis., Proceedings of the National Academy of Sciences of the United States of America, Vol:100, ISSN:0027-8424, Pages:5834-5839
et al., 2003, Telomere attrition and Chk2 activation in human heart failure., Proceedings of the National Academy of Sciences of the United States of America, Vol:100, ISSN:0027-8424, Pages:5378-5383
et al., 2002, Activation and function of cyclin T-Cdk9 (positive transcription elongation factor-b) in cardiac muscle-cell hypertrophy., Nature Medicine, Vol:8, ISSN:1078-8956, Pages:1310-1317
et al., 2002, MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq., Proceedings of the National Academy of Sciences of the United States of America, Vol:99, ISSN:0027-8424, Pages:3866-3871
et al., 2002, Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3., Proceedings of the National Academy of Sciences of the United States of America, Vol:99, ISSN:0027-8424, Pages:2878-2883
et al., 2001, Telomerase reverse transcriptase promotes cardiac muscle cell proliferation, hypertrophy, and survival., Proceedings of the National Academy of Sciences of the United States of America, Vol:98, ISSN:0027-8424, Pages:10308-10313
et al., 2001, Inducible gene targeting in postnatal myocardium by cardiac-specific expression of a hormone-activated Cre fusion protein., Circ Res, Vol:88, Pages:587-592
et al., 2000, TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice., Nature Medicine, Vol:6, ISSN:1078-8956, Pages:556-563
et al., 1998, A Ras-dependent pathway regulates RNA polymerase II phosphorylation in cardiac myocytes: implications for cardiac hypertrophy., Molecular and Cellular Biology, Vol:18, ISSN:0270-7306, Pages:6729-6736
et al., 1997, Adenoviral delivery of E2F-1 directs cell cycle reentry and p53-independent apoptosis in postmitotic adult myocardium in vivo., Journal of Clinical Investigation, Vol:100, ISSN:0021-9738, Pages:2722-2728
et al., 1997, Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo., Journal of Clinical Investigation, Vol:100, ISSN:0021-9738, Pages:169-179
et al., 1993, Highly efficient gene transfer into adult ventricular myocytes by recombinant adenovirus., Journal of Clinical Investigation, Vol:92, ISSN:0021-9738, Pages:381-387
et al., 1991, The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load., Journal of Clinical Investigation, Vol:88, ISSN:0021-9738, Pages:1581-1588
Parker TG, Schneider MD, 1991, Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype., Annual Review of Physiology, Vol:53, ISSN:0066-4278, Pages:179-200
et al., 1990, Differential regulation of skeletal alpha-actin transcription in cardiac muscle by two fibroblast growth factors., Proceedings of the National Academy of Sciences of the United States of America, Vol:87, ISSN:0027-8424, Pages:7066-7070
Schneider MD, Parker TG, 1990, Cardiac myocytes as targets for the action of peptide growth factors., Circulation, Vol:81, ISSN:0009-7322, Pages:1443-1456
Parker TG, Packer SE, Schneider MD, 1990, Peptide growth factors can provoke "fetal" contractile protein gene expression in rat cardiac myocytes., Journal of Clinical Investigation, Vol:85, ISSN:0021-9738, Pages:507-514
et al., 1987, An activated c-Ha-ras allele blocks the induction of muscle-specific genes whose expression is contingent on mitogen withdrawal., Proceedings of the National Academy of Sciences of the United States of America, Vol:84, ISSN:0027-8424, Pages:8956-8960