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Mark Gillespie

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Cardiovascular disease is the leading cause of death in North America. For atherosclerosis, plaque formation in arterial walls occurs as an inflammatory response to high cholesterol, with mature plaques at significant risk for rupture, which not only releases destructive inflammatory mediators into the circulatory system, but can also occlude major arteries resulting in heart attack or stroke. My research focuses on the transcriptional regulatory mechanisms controlling the macrophage response to metabolic changes associated with the progression of atherosclerosis.

Publications Outside of ISB

2010
Scimé A, Soleimani VD, Bentzinger CF, Gillespie, MA, Le Grand F, Grenier G, Bevilacqua L, Harper ME, and Rudnicki MA. (2010) Oxidative status of muscle is determined by p107 regulation of PGC-1a. Journal of Cell Biology. 190:651-662. PMID: 20713602, PMCID: PMC2928004.

2008
Kuang S, Gillespie MA, and Rudnicki MA. (2008) Niche regulation of muscle satellite cell self-renewal and differentiation. Cell Stem Cell. 2:22-31. PMID: 18371418.

2005
Scimé A, Grenier G, Huh MS, Gillespie MA, Bevilacqua L, Harper ME, and Rudnicki MA. (2005) Rb and p107 regulate preadipocyte differentiation into white versus brown fat through repression of PGC-1alpha. Cell Metabolism. 2:283-295. PMID: 16271529.

2004
Gillespie MA, and Rudnicki MA. (2004) Something to SNF about. Nature Genetics. 36:676-677. PMID: 15226749.

ISB Editorial Board: 
Member from August 2013 to Present