Chad Grueter, PhD

Contact Information

Office: 4332 PBDB
Phone: 319-335-3379
Faculty Profile

Brief description of current research:

The basis for the research in my laboratory lies in my strong interest in understanding the transcriptional processes that are disrupted in heart disease. Of particular interest is how cardiac gene expression is altered in obesity and type 2 diabetes and the interplay between the heart and peripheral tissues. We recently identified a novel signaling pathway in the heart that mediates the heart’s ability to regulate global metabolism. Through a combination of pharmacological and genetic gain- and loss-of-function studies in mice, we found the heart is capable of regulating whole body metabolism through a mechanism that is governed by MED13 and miR208a. MED13 is a particularly interesting component of the Mediator complex because it functions as a molecular bridge between the core complex and kinase submodule providing a mechanism for spatial and temporal control of Mediator-dependent regulation of transcription. We use a combination of genetics, proteomics, molecular biology, bioinformatics and biochemistry to study the molecular functions of the Mediator complex in cardiovascular and metabolic disease.

3 most influential diabetes/obesity/metabolism publications:

  • Grueter CE, van Rooij E, Johnson BA, DeLeon SM, Sutherland LB, Qi X, Gautron L, Elmquist JK, Bassel-Duby R, Olson EN. A cardiac microRNA governs systemic energy homeostasis by regulation of MED13. Cell. 2012 Apr 27;149(3):671-83.
  • Carrer M, Liu N, Grueter CE, Williams AW, Frisard MI, Hulver MW, Bassel-Duby R, Olson EN. Control of mitochondrial metabolism and systemic energy homeostasis by microRNAs 378 and 378*. Proc Natl Acad Sci U S A. 2012 Sep 18; 109(38): 15330-5. Epub 2012 Sep 4.
  • Backs J, Thea Backs, Stefan Neef, Michael M. Kreusser, Lorenz H. Lehmann, David M. Patrick, Chad E. Grueter, Xiaoxia Qi, James A. Richardson, Joseph A. Hill, Hugo A. Katus, Rhonda Bassel-Duby, Lars S. Maier and Eric N. Olson. The d isoform of CaM kinase II is required for pathological cardiac hypertrophy and remodeling after pressure overload. Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2342-7. Epub 2009 Jan 28.


It is a funny thing about life; if you refuse to accept anything but the best you very often get it. (W. Somerset Maugham)