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Christopher Cardozo

  • ASSOCIATE PROFESSOR Medicine
  • ASSOCIATE PROFESSOR Pharmacology and Systems Therapeutics
  • ASSOCIATE PROFESSOR Rehabilitation Medicine
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Education

  • M.D., University Wisconsin
    Medicine

  • The Mount Sinai Hospital
    Internal Medicine

  • The Mount Sinai Hospital
    Pulmonary Medicine

  • Mount Sinai School of Medicine

  • B.S., University of Wisconsin
    Mechanical Engineering

Biography

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Research

    The laboratory is a part of the Spinal Cord Damage Research Center, and of the VA Rehabilitation Research and Development Service Center of Excellence located at the Bronx VA Medical Center.  Our work focuses on the biological basis of the loss of muscle and bone that follows spinal cord injury, and on studies of the mechanisms by which androgens and anabolic steroids reduce such loss.  Current investigations in the lab are exploring the role of alterations in signaling through calcineurin, myostatin, PGC-1a, Notch and Wnt in attenuating atrophy caused by paralysis.  We are also characterizing specific molecular events that determine sensitivity of skeletal muscle to androgens focusing on dysregulation of transcriptional coregulators.   A new direction in the laboratory has been characterization of the effects of androgens on bone loss due to paralysis and on unraveling the molecular basis for these actions.  While preliminary, this work is already yielding interesting insights into the utility of these agents to reduce bone loss due to paralysis and elucidating several potential mechanisms related to Wnt and OPG/RANKL signaling.   Another new direction has been to characterize cellular and molecular response of bone and muscle to reloading through use of a novel functional electrical stimulation device developed in collaboration with Dr. Jonathan Jarvis (U. Liverpool, UK) with the hope that such insight will direct choices of therapy to augment gains resulting from reloading of muscle and bone.

Publications

Cardozo CP, Michaud C, Ost MC, Fliss AE, Yang E, Patterson C, Hall SJ, Caplan AJ. Chip Slows Androgen Receptor Synthesis And Reduces Its Rate Of Degradation. Arch Biochem Biophys 2002; 410: 134-140.

Zhao J, Bauman WA, Huang R, Caplan AJ, Cardozo CP. Oxandrolone blocks glucocorticoid signaling in an androgen receptor dependent manner. Steriods 2004; 69(5): 357-66.

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).

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Dr. Cardozo did not report having any of the following types of financial relationships with industry during 2013 and/or 2014: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.

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