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Comparison of Whole Body SOD1 Knockout with Muscle-Specific SOD1 Knockout Mice Reveals a Role for Nerve Redox Signaling in Regulation of Degenerative Pathways in Skeletal Muscle
Author(s) -
Giorgos K. Sakellariou,
Brian McDonagh,
Helen Porter,
Ifigeneia Giakoumaki,
Kate E. Earl,
Gareth Nye,
Aphrodite Vasilaki,
Susan V. Brooks,
Arlan Richardson,
Holly Van Remmen,
Anne McArdle,
Malcolm J. Jackson
Publication year - 2017
Publication title -
antioxidants and redox signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.277
H-Index - 190
eISSN - 1557-7716
pISSN - 1523-0864
DOI - 10.1089/ars.2017.7249
Subject(s) - sod1 , knockout mouse , skeletal muscle , signal transduction , microbiology and biotechnology , superoxide dismutase , anatomy , neuroscience , biology , medicine , endocrinology , receptor , oxidative stress
Lack of Cu,Zn-superoxide dismutase (CuZnSOD) in homozygous knockout mice (Sod1 -/- ) leads to accelerated age-related muscle loss and weakness, but specific deletion of CuZnSOD in skeletal muscle (mSod1KO mice) or neurons (nSod1KO mice) resulted in only mild muscle functional deficits and failed to recapitulate the loss of mass and function observed in Sod1 -/- mice. To dissect any underlying cross-talk between motor neurons and skeletal muscle in the degeneration in Sod1 -/- mice, we characterized neuromuscular changes in the Sod1 -/- model compared with mSod1KO mice and examined degenerative molecular mechanisms and pathways in peripheral nerve and skeletal muscle.

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