Durham, NC 27710
Cardiac rehabilitation and prevention; congestive heart failure; exercise physiology; genetics of cardiovascular disease; coronary heart disease
Dr. Kraus’ research program currently consists of two components: The first is directed at a better understanding of cellular signaling pathways and mechanisms responsible for the adaptive responses of skeletal muscle to normal physiologic stimuli - such as exercise training - and to maladaptive responses to pathophysiologic stimuli -such as in congestive heart failure, skeletal muscle atrophy associated with chronic spaceflight and aging. We are using human studies, animal models and in vitro models of exercise to address these scientific questions. In this work, we have implicated signaling pathways involving cAMP in the responses of skeletal muscle to long term exercise training. We have found that gene expression in skeletal muscle in congestive heart failure is altered in a maladaptive fashion consistent with less effective exercise tolerance and long term disability associated with this condition. We have undertaken exercise training studies in human subjects designed to address questions about mechanisms of exercise training responses in skeletal muscle in normal subjects and those with chronic heart failure. Our in vitro models are designed to explore whether mechanical deformation of skeletal muscle cells (mechanotransduction) are responsible for some of the skeletal muscle responses to changes in contractile activity.
The second area involves human investigations of genetic susceptibility to complex cardiovascular conditions such as coronary artery disease and congestive heart failure. Our goals are several. First is to identify genetic markers that are associated with early onset cardiovascular disease and congestive heart failure so as to be able to better identify high risk subjects and those that may benefit from more aggressive preventive strategies. We also aim to identify causative genetic loci, so as to better understand the etiology and develop new therapeutic strategies for these conditions.
exercise, skeletal muscle, energy metabolism, cell signaling, gene expression, cell stretch, heart failure, aging, spaceflight, human genetics, early onset cardiovascular disease
This faculty member (or a member of their immediate family) has a working relationship (i.e. consulting, research, and/or educational services) with the companies listed below. These relations have been reported to the health system leadership and, when appropriate, management plans are in place to address potential conflicts.
Connelly, JJ; Wang, T; Cox, JE; Haynes, C; Wang, L; Shah, SH; Crosslin, DR; Hale, AB; Nelson, S; Crossman, DC; Granger, CB; Haines, JL; Jones, CJ; Vance, JM; Goldschmidt-Clermont, PJ; Kraus, WE; Hauser, ER; Gregory, SG. GATA2 is associated with familial early-onset coronary artery disease. PLoS Genetics. 2006;2:e139. (2006) Abstract
Huffman, KM; Samsa, GP; Slentz, CA; Duscha, BD; Johnson, JL; Bales, CW; Tanner, CJ; Houmard, JA; Kraus, WE. Response of high-sensitivity C-reactive protein to exercise training in an at-risk population. American Heart Journal. 2006;152:793-800. (2006) Abstract
Duscha, BD; Slentz, CA; Johnson, JL; Houmard, JA; Bensimhon, DR; Knetzger, KJ; Kraus, WE. Effects of exercise training amount and intensity on peak oxygen consumption in middle-age men and women at risk for cardiovascular disease. Chest. 2005;128:2788-2793. (2005) Abstract
Hittel, DS; Kraus, WE; Tanner, CJ; Houmard, JA; Hoffman, EP. Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome. Journal of Applied Physiology. 2005;98:168-179. (2005) Abstract
Slentz, CA; Aiken, LB; Houmard, JA; Bales, CW; Johnson, JL; Tanner, CJ; Duscha, BD; Kraus, WE. Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled study of exercise intensity and amount. Journal of Applied Physiology. 2005;99:1613-1618. (2005) Abstract
Hauser, ER; Crossman, DC; Granger, CB; Haines, JL; Jones, CJ; Mooser, V; McAdam, B; Winkelmann, BR; Wiseman, AH; Muhlestein, JB; Bartel, AG; Dennis, CA; Dowdy, E; Estabrooks, S; Eggleston, K; Francis, S; Roche, K; Clevenger, PW; Huang, L; Pedersen, B; Shah, S; Schmidt, S; Haynes, C; West, S; Asper, D; Booze, M; Sharma, S; Sundseth, S; Middleton, L; Roses, AD; Hauser, MA; Vance, JM; Pericak-Vance, MA; Kraus, WE. A genomewide scan for early-onset coronary artery disease in 438 families: the GENECARD Study. American Journal of Human Genetics. 2004;75:436-447. (2004) Abstract
Houmard, JA; Tanner, CJ; Slentz, CA; Duscha, BD; McCartney, JS; Kraus, WE. Effect of the volume and intensity of exercise training on insulin sensitivity. Journal of Applied Physiology. 2004;96:101-106. (2004) Abstract
Zhang, JS; Kraus, WE; Truskey, GA. Stretch-induced nitric oxide modulates mechanical properties of skeletal muscle cells. American Journal of Physiology: Cell Physiology. 2004;287:C292-C299. (2004) Abstract
Duscha, BD; Annex, BH; Green, HJ; Pippen, AM; Kraus, WE. Deconditioning fails to explain peripheral skeletal muscle alterations in men with chronic heart failure. Journal of the American College of Cardiology. 2002;39:1170-1174. (2002) Abstract
Kraus, WE; Houmard, JA; Duscha, BD; Knetzger, KJ; Wharton, MB; McCartney, JS; Bales, CW; Henes, S; Samsa, GP; Otvos, JD; Kulkarni, KR; Slentz, CA. Effects of the amount and intensity of exercise on plasma lipoproteins. New England Journal of Medicine. 2002;347:1483-1492. (2002) Abstract
Muoio, DM; MacLean, PS; Lang, DB; Li, S; Houmard, JA; Way, JM; Winegar, DA; Corton, JC; Dohm, GL; Kraus, WE. Fatty acid homeostasis and induction of lipid regulatory genes in skeletal muscles of peroxisome proliferator-activated receptor (PPAR) alpha knock-out mice. Evidence for compensatory regulation by PPAR delta. Journal of Biological Chemistry. 2002;277:26089-26097. (2002) Abstract
Muoio, DM; Way, JM; Tanner, CJ; Winegar, DA; Kliewer, SA; Houmard, JA; Kraus, WE; Dohm, GL. Peroxisome proliferator-activated receptor-alpha regulates fatty acid utilization in primary human skeletal muscle cells. Diabetes. 2002;51:901-909. (2002) Abstract