About Dr. Park-Min
Research
Metabolic bone diseases and Inflammatory Bone Destruction
Our research aims to provide a better understanding of bone loss and abnormalities in metabolic bone diseases and bone metabolism in physiological and pathological settings in the field of osteoimmunology. Osteoclasts are of great therapeutic importance for nearly all forms of metabolic bone disease. As such, our lab focuses on investigating new molecular, epigenetic, genetic, and metabolic mechanisms governing the activity of osteoclasts that can be targeted as potential therapeutic strategies for hyperactive osteoclasts in pathological conditions, such as osteoporosis, rheumatoid arthritis, and inflammatory osteolysis. Our lab applies cutting edge cellular and molecular techniques, including genome-wide sequencing, and uses human disease samples and various mouse models to accomplish basic and translational research.
Please see the detailed projects on our lab website: Parkmin Laboratory
Research Interests
- Understanding the molecular and cellular mechanisms of osteoclast differentiation by investigating metabolic reprogramming and epigenetic regulation
- Identifying biomarkers for bone loss in patients with osteoporosis
- Modulating the aberrant activity of osteoclasts and osteoblasts to improve the progression of bone death in patients with avascular necrosis
Credentials
Appointments
Associate Professor, Department of Medicine, Weill Medical College of Cornell University
Associate Scientist, Arthritis and Tissue Degeneration Program, Hospital for Special Surgery
Languages
English
Publications by Dr. Park-Min
Selected Publications
- Mun SH, Bae S, Zeng S, Oh B, Chai C., Kim M, Kim H, Kalliolias G, Dahia C, Oh. Y, Kim T.W., Ji J.D., and Park-Min, K.H. Augmenting MNK1/2 Activation by c-FMS Proteolysis Promotes Osteoclastogenesis and Arthritic Bone Erosion. Bone research 2021 9(1):45
- Bae S, Park PS, Lee YJ, Mun SH, Giannopoulou E, Violante SN, Cross J, and Park-Min, K.H. MYC-mediated early glycolysis negatively regulates proinflammatory responses by controlling IRF4 in inflammatory macrophages. Cell Reports, 2021 35(11) 109264
- A Krez, J Lane, A Helibronner, K.H. Park-Min, K Kaneko, T Pannelini, D Mintz, D. Hansen, DJ McMahon, KA Kirou, G Roboz, P Desai, RS Bockman, and Emily Stein. Risk factors for multi-joint disease in patients with glucocorticoid-induced osteonecrosis. Osteoporosis Internationl 2021 32(10):2095
- Kaneko K, Chen H, Kauffman M., and Park-Min, K.H. Glucocorticoid-induced Osteonecrosis in patients with systemic lupus erythematosus Clinical and translational medicine 2021 11(10):e526
- Mun SH, Jastrzebski S, Kalinowski J., Zeng S., Bae SY, Eugenia G., Khan N., Drissi H., Shin BJ., Lee SK., Lorenzo J.*, and Park-Min, K.H*. Sexual dimorphism in early osteoclasts demonstrates enhanced inflammatory pathway activation in female cells. Journal of Bone and Mineral Research, 2021 36(6) 1104 *co-corresponding author
- Fuji T, Murata K, Mun SH, Bae SY, Lee YJ, Pannellini T, Kang KH, Oliver D, Park-Min, K.H.*, and Ivashkiv L.* MEF2C Regulates Osteoclastogenesis and Pathologic Bone Resorption via c-FOS. Bone research, 2021 11; 9(1):4 *co-corresponding author
- Vertesich V, Sosa B, Niu YZ, Ji G, Turajane K, Mun SH, Xu R, Windhager R, Park-Min, K.H., Greenblatt MB, Bostrom MP, Yang X. Alendronate Enhances Osseointegration in a Murine Implant Model. Journal of Orthopaedic Research, 2021 39(4):719 PMID:32915488
- Park PS, Zeng S, Bae S, and Park-Min, K.H. NRF2 is an upstream regulator of MYC-mediated osteoclastogenesis and pathological bone erosion Cells, 2020 21(9)9: E2133
- Kusnadi A, Park SH, Yuan R, Pannellini T, Giannopoulou E, Oliver D, Lu T, Park-Min KH.*, and Ivashkiv LB*. TNF promotes SREBP activity and binding to inflammatory target genes to regulate macrophage polarization and tissue repair. Immunity. 2019 51(2) *co-corresponding author
- Cao C, Ren Y, Barnett AS, Mirando AJ, Rouse D, Mun SH, Park-Min KH, McNulty AL, Guilak F, Karner CM, Hilton MJ, Pitt GS. Increased Ca2+ signaling through CaV1.2 promotes bone formation and prevent estrogen-deficiency induced bone loss. JCI insight 2017 16;2(22)
- Murata K., Fang C., Terao C., Giannopoulou EG., Lee YJ., Lee MJ., Mun SH., BaeS., Yuan R., Qiao Y., Furu M., Ito H., Ohmura., Matsuda S., Mimori T., Matsuda F., Park-Min KH.*, and Ivashkiv LB*. Integrated regulation of macrophage signalling and cellular metabolism by hypoxia-sensitive COMMD1 suppresses osteoclastogenesis and pathologic bone resoprtion. Immunity.2017. 47(1):66-79. *co-corresponding author
- Bae S., Lee MJ., Mun SH., Giannopoulou., Yong-Gonzalez V., Cross JR., Murata K., Giguère V., van der Meulen M., and Park-Min KH. MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERRα. J. Clin. Invest. 2017.127(7):2555-2568.
- Lee MJ, Lim E, Mun S.-H., Bae S, Murata K, Ivashkiv L, and Park-Min KH. Intravenous Immunoglobulin (IVIG) Attenuates TNF-induced Pathologic Bone Resorption and Suppresses Osteoclastogenesis by Inducing A20 Expression. J Cell Physiol. 2016. 231(2):449-58.
For more publications, please see the PubMed listing.
Industry Relationships
Industry Relationships
One of the goals of HSS is to advance the science of orthopedic surgery, rheumatology, and related disciplines for the benefit of patients. Research staff at HSS may collaborate with outside companies for education, research and medical advances. HSS supports this collaboration in order to foster medical breakthroughs; however, HSS also believes that these collaborations must be disclosed.
As part of the disclosure process, this website lists Research staff collaborations with outside companies if the Research staff member received any payment during the prior year or expects to receive any payment in the next year. The disclosures are based on information provided by the Research staff and other sources and are updated regularly. Current ownership interests and leadership positions are also listed. Further information may be available on individual company websites.
As of April 27, 2020, Dr. Park-Min reported no relationships with healthcare industry.
By disclosing the collaborations of HSS Research staff with industry on this website, HSS and its Research staff make this information available to patients and the public, thus creating a transparent environment for those who are interested in this information. Further, the HSS Conflicts of Interest Policy does not permit payment of royalties on products developed by him/her that are used on patients at HSS.