Simon J. Conway, PhD

Phone: 317-278-8780
Office: R4 402F

Simon J. Conway, PhD

FAHA Professor, Department of Pediatrics

Professor: Department of Pediatrics

Clinical Section: Neonatal-Perinatal Medicine

Basic Science Joint Appointment: Biochemistry and Molecular Biology, Anatomy and Cell Biology, Medical and Molecular Genetics

Member, IU Simon Cancer Center Member



  • Assistant and Associate Professor, Institute of Molecular Medicine & Genetics, Medical College of Georgia
  • PhD: Mammalian Development Unit, Medical Research Council (UK), University College London, England (1993)
  • Postdoctoral Fellowship: Institute of Child Health, Great Ormond Street Children's Hospital, England

Research Interest:

Our lab’s focus is elucidating the underlying mechanisms of impaired cardiopulmonary and nervous system dysfunction in health and disease.  Lack of formation of a separate aorta and pulmonary artery often results in neonatal lethality, and we have established that in neural crest-associated Pax3/7 mutants that this is due to bradycardia/diminished cardiac innervation and associated respiratory failure as there is inappropriate mixing of the oxygenated and de-oxygenated circulations postnatally.  We are currently analyzing key neural crest progenitor effectors that regulate morphogenesis prior to neural crest emigration into the heart. Similarly, these congenital heart defects frequently result in abnormal lung development, including poor alveolar formation leading to Bronchopulmonary dysplasia (BPD).  Using a hyperoxia-induced mouse model of BPD and both Periostin and Tgfbi knockout mice, our lab is examining how initial suppression of TGFbeta superfamily signaling instigates BPD pathogenesis.  To investigate the consequences of TGFbeta superfamily inhibition and to identify specific pathway effectors, we are employing in vivo inducible caNoggin and caSmad7 transgenic as well as Tgfbeta conditional knockout approaches; to either block all combined TGFbeta signaling and then compare these data when only BMP signaling or a single TGFbeta ligand/receptor is deleted.  Abnormal elevated TGFbeta signaling is routinely observed in response to injury and during postnatal cardiopulmonary fibrosis.  Significantly, we have shown that a partial Periostin element is uniquely capable of driving reporter expression in activated cardiac myofibroblasts, providing us with a unique in vivo tool for genetic manipulation of injury-site myofibroblasts.  Thus, we seek to identify the molecular regulators of lineage-specific fibroblast-to-myofibroblast transition in fibrotic lungs and failing hearts and whether these pathological switches can be reversed in vivo.  If these experimentally induced diseases can be prevented and/or nullified in genetically-defined mouse models, we hope to then apply the knowledge gained to help engineer patient treatments.

 A primary responsibility as a principal investigator is the mentoring and advancement of trainees. We have successfully trained and mentored >30 summer interns, undergraduate, MS, PhD and MD/PhD students, as well as postdoctoral and neonatal fellows - hence we are always interested in hearing from motivated candidates  My time is spent primarily on research and we are a very collaborative lab.  We maintain a single purpose, which is to contribute significantly to the current understanding of cardiopulmonary defect pathogenesis and we seek to use basic research to uncover novel therapeutic approaches for the diagnosis and treatment of patients.