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Jingbo Pi
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School of Public Health, China Medical University

Bio: Dr. Pi received M.D. and M.S. on Occupational Health from China Medical University (CMU) and Ph.D. in Medical Sciences from The University of Tsukuba, Japan. He had postdoctoral training at NIEHS, USA (2002-2004) and The Hamner Institutes, USA (2004-2006). He worked as a Research/Assistant/Associate Investigator at The Hamner (2006-2013). In 2013, Dr. Pi was recruited as a professor of CMU, and since then he has been serving as the Dean of School of Public Health. In 2008, Dr. Pi received the ONES Award, NIEHS, USA. His research has been funded by NIDDK (USA), NIEHS (USA), Nature Science Foundation of China and the Ministry of Science and Technology, China. He has authored/co-authored over 200 peer-reviewed papers/book chapters with more than 12,000 citations (H-index 59). Dr. Pi has served as a board member and president/vice president of Stem Cell Specialty Section, SOT, USA and an advisor and subgroup co-chair of IARC/WHO Monographs. Currently, he is an Associate Editor of TAAP, Tox Reports and Toxicological Research, and serves as vice president of multiple Specialty Sections of Chinese SOT. In addition, he functions as the director of the Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China.

 

Abstract: While the CNC-bZIP proteins NRF1 and NRF2 (also known as NFE2L1/2) transcriptionally coordinate multiple stress responses, they play distinct roles in maintaining various cell metabolism and function, including bone remodeling and homeostasis. Here, we aimed to understand the molecular mechanisms underlying osteoporosis induced by prolonged cadmium (Cd) exposure, focusing mainly on the crosstalk between NRF1 and NRF2 in osteoclastogenesis. Using multiple in vivo and in vitro models, we demonstrated that NRF1 functions as a key factor controlling the transcription of Nfatc1/α and osteoclastogenesi in an isoform-specific manner. In contrast, ablation of Nrf2 globally or myeloid-specifically in mice resulted in a relatively minor phenotype in bone metabolism under nonstressed condition, but exacerbated osteoclast activation and bone loss induced by prolonged Cd exposure, suggesting that NRF2-dependent osteoclast homeostasis plays a crucial role against the stressor-induced osteoclast overactivation and osteoporosis. Mechanistic in vitro studies revealed that Nrf2 deficiency aggravates the osteoclast differentiation provoked by low levels of Cd exposure, in which ROS-mediated L-NRF1 activation plays a crucial role in coordinating Nfatc1/α expression and osteoclastogenesis. Together, NRF1 and NRF2 coordinatively respond to Cd exposure and orchestrate osteoclastogenesis. Mismatched and/or imbalanced activation of L-NRF1 and NRF2 in response to the environmental cue may disrupt redox-sensitive signaling leading to impaired bone metabolism and function, bone remodeling in particular.


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Date Time Local Time Room Forum Session Role Topic
2025-10-16 14:00-14:30 2025-10-16,14:00-14:30Room 5 - Guibin Hall 1 Symposium Program (Session)

Session 05: Unlocking the Future of Safety: New Approach Methodologies (NAMs) and Microphysiological Systems (MPS)

Speaker The significance of mechanistic evidence in NGRA: is key characteristics-structuralized NAMs a reasonable approach?
2025-10-17 13:50-14:10 2025-10-17,13:50-14:10Room 2 - Guobin Hall 2 Workshop

Workshop 03: Heavy Metal Toxicity and Human Health-1

Speaker Crosstalk between NRF1 and NRF2 in osteoclastogenesis and osteoporosis induced by prolonged cadmium exposure