Affiliation: UCSD SOM
Professor of Medicine
Phone: 858-552-8585 x3519
Robert A. Terkeltaub, MD, is Chief of Rheumatology at the Veterans Administration Medical Center in San Diego and Professor of Medicine and Associate Division Director at the University of California in San Diego. Dr. Terkeltaub received his medical degree at McGill University in Montreal, Canada, and completed residency and training programs at Montreal General Hospital in Clinical Rheumatology and Internal Medicine. Dr. Terkeltaub has been the recipient of numerous teaching awards at the University of California at San Diego. Dr. Terkeltaub is an Associate Editor of Arthritis and Rheumatism and Current Rheumatology Reports and a member of the NIH Atherosclerosis and Inflammation of the Cardiovascular System Study Section.
Dr. Terkeltaub's research has concentrated principally on inflammation and skeletal biology and the interfaces between the two. Major accomplishments have included the first elucidation of the genetic and molecular etiology of the disease "Idiopathic" Infantile Arterial Calcification as NPP1 deficiency, the first linkage of the chemokines IL-8 and KC/GROalpha to macrophage recruitment in atherosclerosis, detailed elucidation of the molecular pathogenenesis of crystalline-induced joint inflammation, and a series of seminal papers describing the effects of inflammation, inorganic pyrophosphate metabolism and the nucleotide binding and nucleotide pyrophosphosphohydrolytic enzymes TG2 and NPP1, respectively on chondrogenic differentiation and calcification.
Active research programs in the lab include:
*The role of the multiligand receptor RAGE and of the calgranulin family of RAGE ligands in chondrogenic differentiation and cartilage pathology
*The molecular pathology of soft tissue and artery calcification in inorganic pyrophosphate-deficient mice
*The role of TLR-mediated innate immunity in cartilage and synovial joint biology
Current work in the Terkeltaub laboratory also includes studies focused on the tug of war between resting chondrocyte differentiation and maturation to chondrocyte hypertrophy. Chondrocyte hypertrophy mediates osteoarthritis and endochondral calcification mechanisms, we are investigating the molecular pathologic role of transglutaminases TG2 and FXIIIA, and of chemokine receptor signaling, in cartilage biology and in osteoarthritis in specific.
References From PubMed (NCBI)