Shi-Yang Chang

Publications (2)16.4 Total impact

• Article: CORRECTION to: Mitochondrial ferritin attenuates β-amyloid-induced neurotoxicity: reduction in oxidative damage through the Erk/P38 mitogen-activated protein kinase pathways authored by Wu WS, Zhao YS, Shi ZH, Chang SY, Nie GJ, Duan XL, Zhao SM, Wu Q, Yang ZL, Zhao BL, Chang YZ (Antioxid Redox Signal. 18(2):158-69, 2013).

  Wen-Shuang Wu, Ya-Shuo Zhao, Zhenhua Shi, Shi-Yang Chang, Guangjun Nie, Xiang-Lin Duan, Song-Min Zhao, Qiong Wu, Zhen-Ling Yang, Bao-Lu Zhao, Yan-Zhong Chang
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  ABSTRACT: In the original research communication, "Mitochondrial Ferritin Attenuates β-Amyloid-Induced Neurotoxicity: Reduction in Oxidative Damage Through the Erk/P38 Mitogen-Activated Protein Kinase Pathways" by Wen-Shuang Wu et al published in Volume 18, Number 2, pages 158-169, the first micrograph of top line was repeated with the 3rd micrograph of bottom line in Fig. 3Ai. We include a replacement figure and regret for the error.
  Antioxidants & Redox Signaling 02/2013; · 8.20 Impact Factor
• Article: Mitochondrial Ferritin Attenuates β-Amyloid-Induced Neurotoxicity: Reduction in Oxidative Damage Through the Erk/P38 Mitogen-Activated Protein Kinase Pathways.

  Wen-Shuang Wu, Ya-Shuo Zhao, Zhen-Hua Shi, Shi-Yang Chang, Guang-Jun Nie, Xiang-Lin Duan, Song-Min Zhao, Qiong Wu, Zhen-Ling Yang, Bao-Lu Zhao, Yan-Zhong Chang
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  ABSTRACT: Abstract Aims: Mitochondrial ferritin (MtFt), which was recently discovered, plays an important role in preventing neuronal damage in 6-hydroxydopamine-induced Parkinsonism by maintaining mitochondrial iron homeostasis. Disruption of iron regulation also plays a key role in the etiology of Alzheimer's disease (AD). To explore the potential neuroprotective roles of MtFt, rats and cells were treated with Aβ(25-35) to establish an AD model. Results: We report that knockdown of MtFt expression significantly enhanced Aβ(25-35)-induced neurotoxicity as shown by dysregulation of iron homeostasis, enhanced oxidative stress, and increased cell apoptosis. Opposite results were obtained when MtFt was overexpressed in SH-SY5Y cells prior to treatment with Aβ(25-35). Further, MtFt inhibited Aβ(25-35)-induced P38 mitogen-activated protein kinase and activated extracellular signal-regulated kinase (Erk) signaling. Innovation: MtFt attenuated Aβ(25-35)-induced neurotoxicity and reduced oxidative damage through Erk/P38 kinase signaling. Conclusion: Our results show a protective role of MtFt in AD and suggest that regulation of MtFt expression in neuronal cells may provide a new neuroprotective strategy for AD. Antioxid. Redox Signal. 00, 000-000.
  Antioxidants & Redox Signaling 07/2012; · 8.20 Impact Factor