Skeletal muscle satellite cells, mitochondria, and microRNAs: their involvement in the pathogenesis of ALS Tsitkanou, Stavroula, Della Gatta, Paul A and Russell, Aaron P 2016, Skeletal muscle satellite cells, mitochondria, and microRNAs: their involvement in the pathogenesis of ALS, Frontiers in psychology, vol. 7, Article number: 403, pp. 1-9, doi: 10.3389/fphys.2016.00403. Attached Files Name Description MIMEType Size Downloads dellagatta-skeletalmuscle-2016.pdf Published version application/pdf 637.39KB 85 Title Skeletal muscle satellite cells, mitochondria, and microRNAs: their involvement in the pathogenesis of ALS Author(s) Tsitkanou, Stavroula Della Gatta, Paul A orcid.org/0000-0003-2231-8370 Russell, Aaron P orcid.org/0000-0002-7323-9501 Journal name Frontiers in psychology Volume number 7 Season Article number: 403 Start page 1 End page 9 Total pages 9 Publisher Frontiers Research Foundation Place of publication Lausanne, Switzerland Publication date 2016-09-13 ISSN 1664-1078 Keyword(s) skeletal muscle amyotrophic lateral sclerosis satellite cell mitochondria miRNA neuromuscular junction Summary Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease (MND), is a fatal motor neuron disorder. It results in progressive degeneration and death of upper and lower motor neurons, protein aggregation, severe muscle atrophy and respiratory insufficiency. Median survival with ALS is between 2 and 5 years from the onset of symptoms. ALS manifests as either familial ALS (FALS) (~10% of cases) or sporadic ALS (SALS), (~90% of cases). Mutations in the copper/zinc (CuZn) superoxide dismutase (SOD1) gene account for ~20% of FALS cases and the mutant SOD1 mouse model has been used extensively to help understand the ALS pathology. As the precise mechanisms causing ALS are not well understood there is presently no cure. Recent evidence suggests that motor neuron degradation may involve a cell non-autonomous phenomenon involving numerous cell types within various tissues. Skeletal muscle is now considered as an important tissue involved in the pathogenesis of ALS by activating a retrograde signaling cascade that degrades motor neurons. Skeletal muscle heath and function are regulated by numerous factors including satellite cells, mitochondria and microRNAs. Studies demonstrate that in ALS these factors show various levels of dysregulation within the skeletal muscle. This review provides an overview of their dysregulation in various ALS models as well as how they may contribute individually and/or synergistically to the ALS pathogenesis. Language eng DOI 10.3389/fphys.2016.00403 Field of Research 110602 Exercise Physiology 1701 Psychology Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences HERDC Research category C1 Refereed article in a scholarly journal ERA Research output type C Journal article Copyright notice ©2016, The Authors Free to Read? Yes Use Rights Persistent URL http://hdl.handle.net/10536/DRO/DU:30089236 Document type: Journal Article Collections: Faculty of Health Open Access Collection Related Links Link Description Connect to published version Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au. Versions Version Filter Type Thu, 24 Nov 2016, 14:05:52 EST Fri, 25 Nov 2016, 04:01:06 EST Sat, 28 Jan 2017, 05:05:45 EST Fri, 03 Feb 2017, 12:52:54 EST Fri, 03 Feb 2017, 12:59:20 EST Fri, 07 Sep 2018, 12:20:20 EST Filtered Full Citation counts:   Cited 22 times in TR Web of Science Cited 24 times in Scopus Search Google Scholar Access Statistics: 372 Abstract Views, 86 File Downloads  -  Detailed Statistics Created: Thu, 24 Nov 2016, 14:05:52 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.