scispace - formally typeset
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
More filters
Journal ArticleDOI

Osteoclast-Derived Extracellular Vesicles: Novel Regulators of Osteoclastogenesis and Osteoclast-Osteoblasts Communication in Bone Remodeling.

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

Blockade of acid-sensing ion channels protects articular chondrocytes from acid-induced apoptotic injury

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.
Journal ArticleDOI

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.