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| 1 | Estrogen-mediated downregulation of HIF-1αsignaling in B lymphocytes influences postmenopausal bone loss显示文摘In the bone marrow, B cells and bone-resorbing osteoclasts colocalize and form a specific microenvironment. How B cells functionally influence osteoclasts and bone architecture is poorly understood. Using genetically modified mice and highthroughput analyses, we demonstrate that prolonged HIF-1α signaling in B cells leads to enhanced RANKL production and osteoclast formation. In addition, deletion of HIF-1α in B cells prevents estrogen deficiency-induced bone loss in mice.Mechanistically, estrogen controls HIF-1α protein stabilization through HSP70-mediated degradation in bone marrow B cells.The stabilization of HIF-1α protein in HSP70-deficient bone marrow B cells promotes RANKL production and osteoclastogenesis.Induction of HSP70 expression by geranylgeranylacetone(GGA) administration alleviates ovariectomy-induced osteoporosis.Moreover, RANKL gene expression has a positive correlation with HIF1 A expression in human B cells. In conclusion, HIF-1αsignaling in B cells is crucial for the control of osteoclastogenesis, and the HSP70/HIF-1α axis may serve as a new therapeutic target for osteoporosis. | Xianyi Meng Zhen Lin Shan Cao Iga Janowska Koshiro Sonomoto Darja Andreev Knab Katharina Jinming Wen Karl Xaver Knaup Michael Sean Wiesener Gerhard Krönke Marta Rizzi Georg Schett Aline Bozec | 2022 | Bone Research2022，10，2： | 6 |
| 2 | Prospective Study on Circulating MicroRNAs and Risk of Myocardial Infarction显示文摘 | Anna Zampetaki Peter Willeit Lindsey Tilling Ignat Drozdov Marianna Prokopi Jean-Marie Renard Agnes Mayr Siegfried Weger Georg Schett Ajay Shah Chantal M. Boulanger Johann Willeit Philip J. Chowienczyk Stefan Kiechl Manuel Mayr | 2012 | Journal of the American College of Cardiology2012，，： | 2 |
| 3 | Osteoprotegerin Is a Risk Factor for Progressive Atherosclerosis and Cardiovascular Disease显示文摘 | Stefan Kiechl Georg Schett Gregor Wenning Kurt Redlich Martin Oberhollenzer Agnes Mayr Peter Santer Josef Smolen Werner Poewe Johann Willeit | 2004 | Circulation: Journal of the American Heart Association2004，，18： | 2 |
| 4 | New insights in the mechanism of bone loss in arthritis 显示文摘 | Schett Georg Smolen Josef S | 2005 | Curr Pharm Des2005，11，23： | 1 |
| 5 | Dynamic changes in O-GlcNAcylation regulate osteoclast differentiation and bone loss via nucleoporin 153显示文摘Bone mass is maintained by the balance between osteoclast-induced bone resorption and osteoblast-triggered bone formation.In inflammatory arthritis such as rheumatoid arthritis(RA),however,increased osteoclast differentiation and activity skew this balance resulting in progressive bone loss.O-GlcNAcylation is a posttranslational modification with attachment of a single O-linkedβ-D-N-acetylglucosamine(O-GlcNAc)residue to serine or threonine residues of target proteins.Although O-GlcNAcylation is one of the most common protein modifications,its role in bone homeostasis has not been systematically investigated.We demonstrate that dynamic changes in O-GlcNAcylation are required for osteoclastogenesis.Increased O-GlcNAcylation promotes osteoclast differentiation during the early stages,whereas its downregulation is required for osteoclast maturation.At the molecular level,O-GlcNAcylation affects several pathways including oxidative phosphorylation and cell-cell fusion.TNFαfosters the dynamic regulation of O-GlcNAcylation to promote osteoclastogenesis in inflammatory arthritis.Targeted pharmaceutical or genetic inhibition of O-GlcNAc transferase(OGT)or O-GlcNAcase(OGA)arrests osteoclast differentiation during early stages of differentiation and during later maturation,respectively,and ameliorates bone loss in experimental arthritis.Knockdown of NUP153,an O-GlcNAcylation target,has similar effects as OGT inhibition and inhibits osteoclastogenesis.These findings highlight an important role of O-GlcNAcylation in osteoclastogenesis and may offer the potential to therapeutically interfere with pathologic bone resorption. | Yi-Nan Li Chih-Wei Chen Thuong Trinh-Minh Honglin Zhu Alexandru-Emil Matei Andrea-Hermina Györfi Frederic Kuwert Philipp Hubel Xiao Ding Cuong Tran Manh Xiaohan Xu Christoph Liebel Vladyslav Fedorchenko Ruifang Liang Kaiyue Huang Jens Pfannstiel Min-Chuan Huang Neng-Yu Lin Andreas Ramming Georg Schett Jörg H.W.Distler | 2022 | Bone Research2022，10，4： | 1 |
| 6 | Joint remodeling in i~fflammatory disease显示文摘 | Georg Schett | 2007 | Ann Rheum Dis2007，66，： | 1 |
| 7 | Joint remodeling inflammatory disease 显示文摘 | Georg Schett | 2007 | Ann Rheum Dis2007，66，1： | 1 |
| 8 | Animal models of systemic sclerosis : Prospects and limitations 显示文摘 | Christian Beyer Georg Schett Oliver Distler | 2010 | Arthritis Rheu- matology2010，62，10： | 1 |
| 9 | High-Sensitivity C-Reactive Protein and Risk of Nontraumatic Fractures in the Bnmec- k Study显示文摘 | Georg Schett Stefan Kiechl Siegfried Weger | 2006 | 1Archives of internal Medcine2006，22，： | 1 |
| 10 | Molecular mechanisms of inflammatory bone damage:emerging targets for therapy显示文摘 | Sonja Herman Gerhard Kronke Georg Schett | 2008 | Trends Mol Med2008，14，6： | 1 |
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