Christopher Cardozo, MD
- PROFESSOR | Medicine
- PROFESSOR | Rehabilitation and Human Performance
Research Topics:Genetics, Molecular Biology, Muscular Dystrophy, Spinal Cord
Dr. Cardozo is Professor in the Departments of Medicine and Rehabilitation and Human Performance.
He is clinically trained in internal medicine and pulmonary diseases and enzymology of proteases and peptidases. His research seeks to improve function and reduce neuropathological pain in persons with neurological injuries including spinal cord injury. Parallel work investigates the basis for impaired muscle contractile function with aging.
MD, University Wisconsin
The Mount Sinai Hospital
Mount Sinai School of Medicine
The Mount Sinai Hospital
BS, University of Wisconsin
Improving muscle function in older adults and after spinal cord injury. Understanding the impact of common genetic variants on function and pain after spinal cord injury Development of pharmaceuticals to improve physical and metabolic function in immobilized populations
Summary of Research
A major portion of our work aims to discover novel treatments to improve function after paralysis from a spinal cord injury. Other major projects currently being investigated in our lab are:
- Delineating the cellular and molecular roles of Numb and Numb-like in skeletal muscle function.
- Understanding the cellular and molecular basis for the worse outcomes of persons with SCI carrying ApoE4 as compared to ApoE3.
- Testing the role ryanodine receptor dysfunction in skeletal muscle after spinal cord injury and underlying biochemical and molecular mechanisms.
- Systematic studies of the integrative physiology responsible for altered metabolomic profile after spinal cord injury.
Zeman RJ, Zhao J, Zhang Y, Zhao W, Wen X, Wu Y, Pan J, Bauman WA, Cardozo C. Differential skeletal muscle gene expression after upper or lower motor neuron transection. Pflügers Archiv : European journal of physiology 2009 Jul; 458(3).
Wu Y, Zhao W, Zhao J, Zhang Y, Qin W, Pan J, Bauman WA, Blitzer RD, Cardozo C. REDD1 is a major target of testosterone action in preventing dexamethasone-induced muscle loss. Endocrinology 2010 Mar; 151(3).
Wu Y, Bauman WA, Blitzer RD, Cardozo C. Testosterone-induced hypertrophy of L6 myoblasts is dependent upon Erk and mTOR. Biochemical and biophysical research communications 2010 Oct; 400(4).
Qin W, Pan J, Bauman WA, Cardozo CP. Differential alterations in gene expression profiles contribute to time-dependent effects of nandrolone to prevent denervation atrophy. BMC genomics 2010; 11.
Zhao W, Qin W, Pan J, Wu Y, Bauman WA, Cardozo C. Dependence of dexamethasone-induced Akt/FOXO1 signaling, upregulation of MAFbx, and protein catabolism upon the glucocorticoid receptor. Biochemical and biophysical research communications 2009 Jan; 378(3).
Qin W, Pan J, Wu Y, Bauman WA, Cardozo C. Protection against dexamethasone-induced muscle atrophy is related to modulation by testosterone of FOXO1 and PGC-1α. Biochemical and biophysical research communications 2010 Dec; 403(3-4).
Wu Y, Zhao W, Zhao J, Pan J, Wu Q, Zhang Y, Bauman WA, Cardozo CP. Identification of androgen response elements in the insulin-like growth factor I upstream promoter. Endocrinology 2007 Jun; 148(6).
Zhao J, Zhang Y, Zhao W, Wu Y, Pan J, Bauman WA, Cardozo C. Effects of nandrolone on denervation atrophy depend upon time after nerve transection. Muscle & nerve 2008 Jan; 37(1).
Zhao W, Pan J, Zhao Z, Wu Y, Bauman WA, Cardozo CP. Testosterone protects against dexamethasone-induced muscle atrophy, protein degradation and MAFbx upregulation. The Journal of steroid biochemistry and molecular biology 2008 May; 110(1-2).
Zhao W, Pan J, Wang X, Wu Y, Bauman WA, Cardozo CP. Expression of the muscle atrophy factor muscle atrophy F-box is suppressed by testosterone. Endocrinology 2008 Nov; 149(11).