Dr. Correll is an assistant professor in the Department of Biological Sciences in the University of Alabama College of Arts and Sciences, and an associate scientist of the Comprehensive Cardiovascular Center of the University of Alabama at Birmingham. He has extensive expertise in mouse genetic models and surgical techniques that his lab employs to understand the molecular mechanisms involved in the development and progression of heart failure.
Representative Publications
- Overlapping and differential functions of ATF6α versus ATF6β in the mouse heart. R.N. Correll, K.M. Grimes, V. Prasad, J.M. Lynch, H. Khalil, J.D. Molkentin. Sci Rep. 9: 2059, 2019.
- Mitsugumin 29 regulates t-tubule architecture in the failing heart. R.N. Correll, J.M Lynch, T.G. Schips, V. Prasad, A.J. York, M.A. Sargent, D.X.P. Brochet, J. Ma, J.D. Molkentin. Sci Rep. 7: 5328, 2017.
- A Tension-Based Model Distinguishes Hypertrophic versus Dilated Cardiomyopathy. J. Davis, L.C. Davis, R.N. Correll, C.A. Makarewich, J.A. Schwanekamp, F. Moussavi-Harami, D. Wang, A.J. York, H. Wu, S.R. Houser, C.E. Seidman, J.G. Seidman, M. Regnier, J.M. Metzger, J.C. Wu, J.D. Molkentin. Cell. 165: 1147-1159, 2016.
- STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy. R.N. Correll, S.A. Goonasekera, J.H. van Berlo, A.R. Burr, F. Accornero, H. Zhang, C.A. Makarewich, A.J. York, M.A. Sargent, X. Chen, S.R. Houser, J.D. Molkentin. J Mol Cell Cardiol. 87: 38-47, 2015.
- Overexpression of the Na+/K+ ATPase α2 but not α1 isoform attenuates pathological cardiac hypertrophy and remodeling. R.N. Correll, P. Eder, A.R. Burr, S. Despa, J. Davis, D.M. Bers, J.D. Molkentin. Circ Res. 114: 249-256, 2014.
Research Interests
In the Correll Lab, our major research interests are the molecular processes that underlie the pathogenesis and progression of cardiac disease, with a focus on understanding a) how unfolded protein response (UPR) signaling and b) dysregulation of calcium handling control remodeling of the heart after acute injury or chronic stress. Our recent work identified that UPR signaling through the ATF6 transcription factor is essential for compensatory remodeling in response to hemodynamic stress, such as chronic hypertension. Ongoing studies in the Correll Lab seek to understand the cell-type specific ATF6 signaling that occurs during disease, as well as elucidate mechanisms that control ATF6 activation in the heart.
