Molecular Musculoskeletal


Christopher Cardozo, MD.
VA RR&D National Center of Excellence
for the Medical Consequences of Spinal Cord Injury
Jame J. Peters VAMC, Bronx, New York

(718) 584-9000 ext 1828

Dr. Cardozo has an undergraduate degree in Mechanical Engineering and received his medical degree from University of Wisconsin. He completed his residency in Internal Medicine and Fellowship in Pulmonary Diseases at Mount Sinai School of Medicine. His early work sought to better understand the causes of damage to the lungs after trauma or in a disease called emphysema. Emphysema is caused by an inappropriate breakdown of elastic proteins in the lungs. To further his interest in the biochemistry by which proteins are attacked by cells, he worked for ten years on the proteasome, an intracellular protease (enzyme) in the laboratory of Dr. Marian Orlowski, who together with Sherwin Wilk, discovered the proteasome enzyme. This cellular machine breaks down proteins to dispose of the damaged ones and regulate cellular function.

In 2001, Dr. Cardozo joined the Spinal Cord Damage Research Center to investigate how androgens reduce loss of muscle size and function after a spinal cord injury. While working in the Spinal Cord Damage Research Center, Dr. Cardozo and his team of scientists have, and hope to continue, to advance the understanding of both causes of muscle weakness and possible treatments that might prevent or reverse it. 

Program goals (Lay)
Due to a reduced or complete lack of physical activity for those with a spinal cord injury, the unused muscle becomes more easily fatigued and atrophies. Reduced muscle activity causes the bones associated with them to become weaker, more brittle and susceptible to fracture.     In order to gain a better understanding of why the muscle shrinks and the bones become brittle, Dr. Cardozo and his team have focused their research to answer the questions about changes in muscle and bone function after a spinal cord injury. He and his colleagues are trying to better understand how bone and muscle communicate between each other in normal states and after spinal cord injury. Through his work in the laboratory, Dr. Cardozo and his team are studying the potential of innovative mechanical interventions and the administration of novel drugs to improve the function of paralyzed muscle.

With an improved understanding of the way that bones deteriorate over time after paralysis, he and his team are actively working with clinician investigators and pharmaceutical companies to create novel drugs to prevent or slow the deterioration of muscle and bone and, possibly, to assist in restoring muscle and bone mass and strength.

Program goals (Scientific)
Dr. Cardozo’s interests are in the biology of muscle dysfunction and adaptation to changes in workload with a particular emphasis on transcriptional regulation, changes in the transcriptome, and identification of novel roles for previously identified signaling pathways.
One major research area focuses on determining the molecular mechanisms by which androgens reduce muscle atrophy caused by paralysis. Currently, these studies focus on the role of Numb in skeletal muscle and of increased expression of Numb in preventing skeletal muscle atrophy.

A highly novel area of investigation that is being pursued is the endocrine and paracrine functions of skeletal muscle. These studies use primary cultures of muscle fibers to isolate and identify substances secreted from muscle, and to identify biological activity of these products on nearby nerve and muscle stem cells. Model systems have been developed by which one can identify and characterize the function of substances that act locally on brain, bones, pancreas, and fat.

A new avenue of pre-clinical investigation is to gain insight into the function and molecular aspects of the intersection between aging and spinal cord injury. Novel pharmaceutical approaches that might mitigate the adverse effects of deterioration in muscle function with age after a spinal cord injury are anticipated to be tested in the near future.



Relevant Publications

1. Wu Y, Zhao J, Zhao W, Pan J, Bauman WA, Cardozo CP.
J Neurotrauma. 2012 May 20;29(8):1663-75. Nandrolone normalizes determinants of muscle mass and fiber type after spinal cord injury. PMID 22208735
2. Liu XH, Yao S, Qiao RF, Levine AC, Kirschenbaum A,
Pan J, Wu Y, Qin W, Bauman WA, Cardozo CP. Nandrolone reduces activation of Notch signaling in denervated muscle associated with increased Numb expression. Biochem Biophys Res Commun. 2011 Oct 14;414(1):165-9. PMID: 21945932  
3. Wu Y, Collier L, Pan J, Qin W, Bauman WA, Cardozo CP
Spinal Cord. Testosterone reduced methylprednisolone-induced muscle atrophy in spinal cord-injured rats. 2012 Jan;50(1):57-62. PMID: 21931329  

For a full listing of publications, please see: