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Calogera M Simonaro, PhD
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About Me
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Position
Research Topics
Apoptosis/Cell Death, Biomechanics/Bioengineering, Bone Biology, Cartilage Biology, Cellular Differentiation, Cytokines, Genetics, Inflammation, Lysosomal Storage Diseases, Pathology
About Me
Language
Position
Research Topics
Apoptosis/Cell Death, Biomechanics/Bioengineering, Bone Biology, Cartilage Biology, Cellular Differentiation, Cytokines, Genetics, Inflammation, Lysosomal Storage Diseases, Pathology
About Me
Language
Position
Research Topics
Apoptosis/Cell Death, Biomechanics/Bioengineering, Bone Biology, Cartilage Biology, Cellular Differentiation, Cytokines, Genetics, Inflammation, Lysosomal Storage Diseases, Pathology
Education
BA, St. John's University
MS, Brooklyn College
PhD, New York University
, Mount Sinai School of Medicine
MPh, New York University
Research
Postdoctoral Fellows: Michael Frobergh
Research Personnel: Research Assistant: Yi Ge, Fanli Meng, Changzhi Zhu
The overall goal of our research is to fill the void in our understanding of MPS bone and joint disease and to develop new and improved therapies that might benefit MPS patients. We specifically study two animal models with MPS VI, but anticipate that the results obtained can be applicable to the general class of MPS disorders and benefit a wide range of patients.
Our studies carried out over the past five years have revealed that glycosaminoglycan GAG accumulation is a direct cause of chondrocyte death (apoptosis) in the articular cartilage and growth plates of MPS animals, leading to abnormal matrix homeostasis. This enhanced cell death also triggers a series of signaling events that lead to marked inflammatory disease with characteristic increases in proinflammatory cytokines, metalloproteinases (MMPs), and apoptotic cells. Together, these two factors (enhanced cell death and inflammation), lead to the characteristic bone and joint disease in the MPS disorders. In addition, cellular defects associated with the maturation of MPS growth plates are likely contributing to abnormal bone growth.
Locations
Publications
Recent Artifacts
- New paradigms for the treatment of lysosomal storage diseases: targeting the endocannabinoid system as a therapeutic strategy
- Acid Ceramidase Protects Against Hepatic Ischemia/Reperfusion Injury by Modulating Sphingolipid Metabolism and Reducing Inflammation and Oxidative Stress
- A New Fluorescent Method to Detect Sulfamidase Activity in Blood, Tissue Extracts and Dried Blood Spots
- Growth plate pathology in the mucopolysaccharidosis type VI rat model-an experimental and computational approach
- Safety study of sodium pentosan polysulfate for adult patients with mucopolysaccharidosis Type II
- Efficacy of pentosan polysulfate in in vitro models of lysosomal storage disorders: Fabry and Gaucher Disease
- Pentosan polysulfate treatment of mucopolysaccharidosis type IIIA mice
- Enzyme replacement therapy for Farber disease: Proof-of-concept studies in cells and mice
- Treatment with pentosan polysulphate in patients with MPS I: results from an open label, randomized, monocentric phase II study
- The Genetics of Sphingolipid Hydrolases and Sphingolipid Storage Diseases