ICMRS Scientific Frontier Webinar Series
Metabolic Bone Diseases: The Clinical and Pathogenesis
Presented by Xianghang Luo, Ph.D.
Professor and Director of Department of Endocrinology at the Xiangya Hospital of Central South University
When: August 1, 2020 (Saturday) 9:00 PM Eastern Time (US and Canada)
August 1, 2020 (Saturday) 8:00 PM Central Time (US and Canada)
August 2, 2020 (Sunday) 9:00 AM Perth (Australia - Western Australia)
August 2, 2020 (Sunday) 11:00 AM Sydney (Australia - New South Wales)
Where: Please click here to view the recorded webinar.
Short Biography: Dr. Xianghang Luo is Professor and Director of Department of Endocrinology at the Xiangya Hospital of Central South University, supported by the National Science Fund for Distinguished Young Scholars. One of his major research projects focuses on the mechanism of bone metabolism disease. Dr. Luo is a member of Chinese Society of osteoporosis and bone mineral research and fellow of the American Society for Bone and Mineral Research (ASBMR).
Abstract: Metabolic bone diseases are bone metabolic disorder mainly manifested as abnormality of bone growth and development, structural morphology and biochemical indicators caused by bone modeling/remodeling disorder. In severe cases, there may be bone malformation or fracture. The etiology and clinical manifestations of many metabolic bone diseases are unknown, so understanding these diseases is important for the clinical diagnosis and treatment.
Based on rare endocrine diseases, our study identified the pathogenic gene Reg1cp of high bone mass syndrome in the population with high bone mass syndrome and found its target KLF3. Through screening, we concluded that the antagonist of KLF3, Ophiopogonin D, could promote bone formation, providing a new way for the osteoporosis treatment. Osteoporosis is a common metabolic bone disease, mainly manifested as bone aging. As the endocrine center, hypothalamus plays an important role in the process of bone aging. We found that Hnscr, a gene highly expressed in hypothalamus neural stem cells, decreases with age. Hnscr inhibits senescence gene expression by stabilizing YB-1 structure. Hnscr depletion can induce senescence of hypothalamic neural stem cells and induce bone senescence phenotype. The tea extract Theaflavin 3-Gallate was identified to simulate the function of Hnscr and slow down the aging process of mice bone by maintaining the vitality of hypothalamus stem cells. In conclusion, the discovery of the mechanism of metabolic bone disease plays a key role in promoting the clinical diagnosis and treatment. The clinical and mechanism are the cornerstones of each other, promoting the steady development of metabolic bone disease.This webinar will be moderated by Dr. Ge Zhang, Professor of Chinese Medicine and Director of Institute for Advancing Translational Medicine in Bone and Joint Diseases, Hong Kong Baptist University.
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For more information, please contact:
Jean Jiang, PhD
Chair, Education Committee, ICMRS
Professor and Zachry Distinguished University Chair
Department of Biochemistry and Structural Biology
University of Texas Health Science Center at San AntonioEmail: firstname.lastname@example.org