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Opposing roles of miR-21 and miR-29 in the progression of fibrosis in Duchenne muscular dystrophy.

Zanotti S1, Gibertini S1, Curcio M1, Savadori P1, Pasanisi B1, Morandi L1, Cornelio F1, Mantegazza R1, Mora M2.
Biochimica et biophysica acta.Biochim Biophys Acta.2015 Jul;1852(7):1451-64. doi: 10.1016/j.bbadis.2015.04.013. Epub 2015 Apr 17.
Excessive extracellular matrix deposition progressively replacing muscle fibres is the endpoint of most severe muscle diseases. Recent data indicate major involvement of microRNAs in regulating pro- and anti-fibrotic genes. To investigate the roles of miR-21 and miR-29 in muscle fibrosis in Duchenne
PMID 25892183

Altered ROS production, NF-κB activation and interleukin-6 gene expression induced by electrical stimulation in dystrophic mdx skeletal muscle cells.

Henríquez-Olguín C1, Altamirano F2, Valladares D3, López JR4, Allen PD4, Jaimovich E5.
Biochimica et biophysica acta.Biochim Biophys Acta.2015 Jul;1852(7):1410-9. doi: 10.1016/j.bbadis.2015.03.012. Epub 2015 Apr 7.
Duchenne muscular dystrophy is a fatal X-linked genetic disease, caused by mutations in the dystrophin gene, which cause functional loss of this protein. This pathology is associated with an increased production of reactive oxygen (ROS) and nitrogen species. The aim of this work was to study the alt
PMID 25857619

Metformin increases peroxisome proliferator-activated receptor γ Co-activator-1α and utrophin a expression in dystrophic skeletal muscle.

Ljubicic V1, Jasmin BJ1.
Muscle & nerve.Muscle Nerve.2015 Jul;52(1):139-42. doi: 10.1002/mus.24692. Epub 2015 May 14.
INTRODUCTION: Metformin (MET) stimulates skeletal muscle AMP-activated protein kinase (AMPK), a key phenotype remodeling protein with emerging therapeutic relevance for Duchenne muscular dystrophy (DMD). Our aim was to identify the mechanism of impact of MET on dystrophic muscle.METHODS: We investig
PMID 25908446