Peter S. Rabinovitch
Ph.D., University of Washington, Genetics, 1980.
M.D., University of Washington, Medicine, 1979.
The focus of the laboratory is upon studies of DNA damage and genomic instability in aging and in neoplastic progression. In aging, we are interested in the connection between DNA damage and free radical injury and lifespan and disease. Transgenic mice that overexpress antioxidant enzymes have enhanced longevity and are being examined to provide insights in this model system. In particular, mice hat overexpress catalase targeted to mitochondria have extended longevity, and healthspan - the latter includes resistance to cardiac aging and experimental heart disease, reduced sarcopenia, and resistance to non-hematological malignancies. Studies of neoplastic progression focus on human gastrointestinal cancers and precancerous diseases such as Ulcerative Colitis. A better understanding of neoplastic progression in these diseases may yield biomarkers of increased clinical risk for progression to cancer. Genomic instability has proven to be one such a marker. In both aging and neoplasia, we are interested in the role of telomere shortening in promoting genomic instability. Additional molecular genetic and cytometric indicators of genomic instability and DNA repair are being studied.
Director, University of Washington Nathan Shock Center of Excellence in the Basic Biology of Aging
Director, University of Washington Genetic Approaches to Aging Training Grant
Director, Anatomic Pathology Flow Cytometry Laboratory, University of Washington Medical Center
International Society for Analytical Cytology
DNA Libraries (Methods for making and using single-chromosome amplification libraries, Patent Number: 5814444, , , United States of America.
Reducing mTOR Augments Parietal Epithelial Cell Density in a Model of Acute Podocyte Depletion and in Aged Kidneys.. American journal of physiology. Renal physiology. :ajprenal.00196.2016.. 2016.
AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia.. Journal of molecular and cellular cardiology. 91:104-13.. 2016.
The Aging Heart.. Cold Spring Harbor perspectives in medicine. 5(9). 2015.
Respiratory chain protein turnover rates in mice are highly heterogeneous but strikingly conserved across tissues, ages, and treatments.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology.. 2015.
Mitochondrial dysfunction in cardiac aging.. Biochimica et biophysica acta.. 2015.
Quality control systems in cardiac aging.. Ageing research reviews.. 2015.
Healthy aging: The ultimate preventative medicine.. Science (New York, N.Y.). 350(6265):1191-3.. 2015.
Dose-dependent effects of mTOR inhibition on weight and mitochondrial disease in mice.. Frontiers in genetics. 6:247.. 2015.
"Indefinite for Dysplasia" in Barrett's Esophagus: Inflammation and DNA Content Abnormality are Significant Predictors of Early Detection of Neoplasia.. Clinical and translational gastroenterology. 6:e81.. 2015.
Macrophage Mitochondrial Oxidative Stress Promotes Atherosclerosis and Nuclear Factor-κB-Mediated Inflammation in Macrophages.. Circulation research. 114(3):421-33.. 2014.
Mitochondrial oxidative stress in aging and healthspan.. Longevity & healthspan. 3:6.. 2014.
Global proteomics and pathway analysis of pressure-overload-induced heart failure and its attenuation by mitochondrial-targeted peptides.. Circulation. Heart failure. 6(5):1067-76.. 2013.
Preserving youth: does rapamycin deliver? Science translational medicine. 5(211):211fs40.. 2013.
Clonal Expansions and Short Telomeres Are Associated with Neoplasia in Early-onset, but not Late-onset, Ulcerative Colitis.. Inflammatory bowel diseases. 19(12):2593-602.. 2013.
mTOR is a key modulator of ageing and age-related disease.. Nature. 493(7432):338-45.. 2013.
mTOR inhibition alleviates mitochondrial disease in a mouse model of Leigh syndrome.. Science (New York, N.Y.). 342(6165):1524-8.. 2013.