Simon J. Conway

Indiana University School of Medicine

Medicine · Health Sciences

83h-index30.3kcitations338works3.12yr avg
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Research Topics

Cardiac Fibrosis and Remodeling(77), Congenital heart defects research(76), Signaling Pathways in Disease(39), Peptidase Inhibition and Analysis(26), Tissue Engineering and Regenerative Medicine(23)

Publications338 total

BACH2 links β1-adrenergic receptor/β-arrestin1 signaling to MIAT to inhibit cardiac fibroblast activation and cardiomyocyte apoptosis
Cell Death Discovery·2026Open Access
MEK inhibitor Mirdametinib promotes fracture healing in osteofibrous dysplasia RASopathy
Journal of Clinical Investigation·2026Open Access
A transcriptional code controlling fluid shear stress-induced gene expression
2026
Focused ultrasound-mediated drug delivery of bevacizumab in treating NF2-related schwannomatosis in an animal model
Scientific Reports·2025Open Access
Deficient Cardiolipin Remodeling Alters Muscle Fiber Composition and Neuromuscular Connectivity in Barth Syndrome
2025Open Access
Periostin promotes inflammation and neovascularization in atopic keratoconjunctivitis
Journal of Allergy and Clinical Immunology·2025Open Access
Correction to: Granulopoietic Dysregulation in a Patient-Tailored Mouse Model of Barth Syndrome
Stem Cell Reviews and Reports·2025Open Access
Focused ultrasound-mediated drug delivery of bevacizumab in treating NF2-related schwannomatosis in an animal model
2025Open Access
Granulopoietic Dysregulation in a Patient-Tailored Mouse Model of Barth Syndrome
Stem Cell Reviews and Reports·2025· 1 citedOpen Access
Correction to: Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart
Circulation Research·2025
Cardiomyocyte-restricted MIAT deletion is sufficient to protect against murine myocardial infarction
Cell Death Discovery·2025· 2 citedOpen Access
Serum Periostin is Able to Stratify Type 2-Dominant Ulcerative Colitis
Inflammatory Bowel Diseases·2025· 2 citedOpen Access
What can ATP content tell us about Barth syndrome muscle phenotypes?
Journal of Translational Genetics and Genomics·2025· 5 citedOpen Access
The Loss of Tafazzin Transacetylase Activity Is Sufficient to Drive Testicular Infertility
Journal of Developmental Biology·2024· 3 citedOpen Access
Spatial transcriptomics of human and murine Neurofibromatosis Type I fracture pseudarthroses reveal impaired BMP signaling
American Journal of Clinical Pathology·2024Open Access
A Barth Syndrome Patient-Derived D75H Point Mutation in TAFAZZIN Drives Progressive Cardiomyopathy in Mice
International Journal of Molecular Sciences·2024· 6 citedOpen Access
Spatial transcriptomics implicates impaired BMP signaling in NF1 fracture pseudarthrosis in murine and patient tissues
JCI Insight·2024· 9 citedOpen Access
Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart
Circulation Research·2024· 27 citedOpen Access
Cavin-2 Promotes Fibroblast-to-Myofibroblast Trans-Differentiation and Aggravates Cardiac Fibrosis
ESC Heart Failure·2023· 13 citedOpen Access
SPRR1A is a key downstream effector of MiR-150 during both maladaptive cardiac remodeling in mice and human cardiac fibroblast activation
Cell Death and Disease·2023· 15 citedOpen Access
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Frequent Co-authors

Roger R. Markwald(6), Rhonda Rogers(6), Mervin C. Yöder(5), Paige Snider(5), Kenji Izuhara(4), Agnieszka Kruzynska‐Frejtag(4), Xiang Wu(4), Frederick H. Leibach(4), Vadivel Ganapathy(4), Jeffery D. Molkentin(3), Kathleen E. McGrath(3), James Palis(3), Manabu Maeda(3), Wei Huang(3), Momoko Yoshimoto(3), Florent Ginhoux(2), Melanie Greter(2), Marylène Leboeuf(2), Peter See(2), Lai Guan Ng(2)