Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype-Reference-Cited by-同舟云学术

Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype

Published:2015-08 Issue: Volume:5 Page:140-148
ISSN:2213-2317
Container-title:Redox Biology
language:en
Short-container-title:Redox Biology

Author:

Sataranatarajan Kavithalakshmi,Qaisar Rizwan,Davis Carol,Sakellariou Giorgos K.,Vasilaki Aphrodite,Zhang Yiqiang,Liu Yuhong,Bhaskaran Shylesh,McArdle Anne,Jackson Malcolm,Brooks Susan V.,Richardson Arlan,Van Remmen Holly

Funder

NIH/NIA

Veterans Affairs Merit Grant

Publisher

Elsevier BV

Subject

Organic Chemistry,Biochemistry,Clinical Biochemistry

Reference28 articles.

1. Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy;Muller;Free Radical Biology and Medicine,2006

2. Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration;Jang;FASEB Journal,2010

3. Skeletal muscle weakness due to deficiency of CuZn-superoxide dismutase is associated with loss of functional innervation;Larkin;American Journal of Physiology – Regulatory, Integrative and Comparative Physiology,2011

4. Neuron-specific expression of CuZnSOD prevents the loss of muscle mass and function that occurs in homozygous CuZnSOD-knockout mice;Sakellariou;FASEB Journal,2014

5. CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice;Zhang;FASEB Journal,2013

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