Duchenne muscular dystrophy (DMD) causes progressive muscle weakness. There is currently no cure for the disease; however, recent studies have suggested that a bioactive lipid, sphingosine-1-phosphate (S1P), might protect against eventual muscle degeneration. S1P is an inhibitor of histone deacetylases (HDACs), which could form the molecular basis of its protective role in DMD. To test this possibility, Hannele Ruohola-Baker and colleagues exploited Drosophila and mouse models of the disease. They reduced levels of Rpd3, the Drosophila homologue of HDAC2, and found that disease symptoms were alleviated. In DMD mice, symptoms were also improved upon treatment with a compound that increases levels of S1P and suppresses HDAC activity. Interestingly, this improvement correlated with the expression of two miRNAs involved in promoting regeneration and energy metabolism in skeletal muscle tissue. This cross-species analysis thereby provides important insights into the pathology of DMD and the therapeutic potential of S1P. Page
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January 2014
Development/DMM Virtual Meeting 2021
Welcoming new Editors to DMM
Editor-in-Chief Liz Patton wants DMM to strengthen its presence in the field of translational biology and to focus on the importance of disease mechanisms, just as much as models. To implement this vision, we are pleased to welcome new Editors Sally Dunwoodie (Victor Chang Cardiac Research Institute, Australia), Monkol Lek (Yale School of Medicine, USA) and Rickie Patani (Francis Crick Institute, London, UK) to the team.
Roles of the gut microbiome in colorectal cancer development
Going hand-in-hand, a new Perspective by Foegeding et al. explores the Western diet as a driver of dysbiosis in colorectal cancer while a new Review by Wang et al. focuses on microbiota-driven mechanisms that initiate sporadic colorectal cancer.
preLights – the latest disease modelling preprints
Head over to preLights for the digests of the latest preprints:
Erin McGregor highlights work by Nowicka et al. that suggests a potential connection between mitochondrial dysfunction and neurodegeneration.
Emma Wilson discusses work by Dagra et al., which highlights D2 receptors as a potential target that could be used to alleviate alpha-Synuclein pathology in Parkinson’s disease.
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