F
Feng-Lai Yuan
Researcher at Nantong University
Publications - 63
Citations - 907
Feng-Lai Yuan is an academic researcher from Nantong University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 16, co-authored 45 publications receiving 664 citations. Previous affiliations of Feng-Lai Yuan include Anhui Medical University & Nanjing University of Chinese Medicine.
Papers
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Journal ArticleDOI
Osteoclast-Derived Extracellular Vesicles: Novel Regulators of Osteoclastogenesis and Osteoclast-Osteoblasts Communication in Bone Remodeling.
Feng-Lai Yuan,Qian-Yuan Wu,Zong-Ning Miao,Ming-Hui Xu,Rui-Sheng Xu,Dong-Lin Jiang,Jun-Xing Ye,Fei-Hu Chen,Mingdong Zhao,Hao-Jue Wang,Xia Li +10 more
TL;DR: Recent advances in the field of osteoclast-derived EVs in bone remodeling regulation are reviewed, summarizing a new regulator of osteoporosis and osteOClast–osteoblast communication mediated by osteoc Last- derived EVs.
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Leonurine hydrochloride inhibits osteoclastogenesis and prevents osteoporosis associated with estrogen deficiency by inhibiting the NF-κB and PI3K/Akt signaling pathways
TL;DR: In this study, LH suppressed RANKL-induced osteoclastogenesis via RANK-TRAF6, NF-κB, and PI3K/Akt signaling, thus preventing bone loss caused by estrogen deficiency in mice and providing the first evidence that LH might be a promising therapeutic compound to treat osteoporosis.
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The Roles of Acidosis in Osteoclast Biology.
TL;DR: The recent investigations into the effects of acidosis in osteoclast biology and the acid-sensing molecular mechanism are discussed.
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Blockade of acid-sensing ion channels protects articular chondrocytes from acid-induced apoptotic injury
Wei Hu,Fei-Hu Chen,Feng-Lai Yuan,Feng-Lai Yuan,Teng-Yue Zhang,Fan-rong Wu,Chao Rong,Sheng Jiang,Jie Tang,Cheng-Cheng Zhang,Mei-Ying Lin +10 more
TL;DR: Experimental evidence is provided that blocking ASICs could protect acid-induced apoptotic injury to chondrocytes and reduce the cell death percentage and increased cell viability following acid exposure.
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Induction of autophagy by salidroside through the AMPK-mTOR pathway protects vascular endothelial cells from oxidative stress-induced apoptosis.
TL;DR: Autophagy is a protective mechanism in HUVECs under oxidative stress and that salidroside might promote autophagy through activation of the AMPK pathway and downregulation of mTOR pathway.