scispace - formally typeset
Y

Yuechen Han

Researcher at Shandong University

Publications -  67
Citations -  870

Yuechen Han is an academic researcher from Shandong University. The author has contributed to research in topics: Facial nerve & Spiral ganglion. The author has an hindex of 13, co-authored 60 publications receiving 611 citations.

Papers
More filters
Journal ArticleDOI

Wnt Signaling Activates TP53-Induced Glycolysis and Apoptosis Regulator and Protects Against Cisplatin-Induced Spiral Ganglion Neuron Damage in the Mouse Cochlea

TL;DR: This study is the first to indicate that Wnt signaling activates TIGAR and protects SGNs against cisplatin-induced damage through the inhibition of oxidative stress and apoptosis in S GNs, and this might offer novel therapeutic targets for the prevention of SGN injury.
Journal ArticleDOI

PRDX1 activates autophagy via the PTEN-AKT signaling pathway to protect against cisplatin-induced spiral ganglion neuron damage.

TL;DR: In this article, the effect of autophagy on cisplatin-induced SGN injury is investigated, and it was shown that autophagic flux was activated in SGNs after cisplatal damage, whereas these were exacerbated by the autophag inhibitor 3-methyladenine.
Journal ArticleDOI

The Three-Dimensional Culture System with Matrigel and Neurotrophic Factors Preserves the Structure and Function of Spiral Ganglion Neuron In Vitro

TL;DR: 3D culture system preserves the structure and function of SGN in explant culture and combined with neurotrophic factors had accumulated effects in promoting the neurites outgrowth compared with 3D culture or NFs treatment only groups.
Journal ArticleDOI

c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro.

TL;DR: Evidence is provided that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss by knocking down c- myb expression with shRNA transfection in HEI-OC1 cells and finding that c -Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult.