Results 1 to 10 of about 9,256 (223)
GsMTx4-D provides protection to the D2.mdx mouse. [PDF]
Duchenne muscular dystrophy is a life-limiting muscle disease that has no current effective therapy. Despite mounting evidence that dysregulation of mechanosensitive ion channels is a significant contributor to dystrophy pathogenesis, effective pharmacologic strategies targeting these channels are lacking.
Ward CW, Sachs F, Bush ED, Suchyna TM.
europepmc +6 more sources
Summary: The DBA/2J (D2) mdx mouse is a more severe model of Duchenne muscular dystrophy when compared to the traditional C57BL/10 (C57) mdx mouse. Here, we questioned whether sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) function would differ in ...
Riley E.G. Cleverdon +8 more
doaj +1 more source
Skeletal muscle fibrosis in the mdx/utrn+/- mouse validates its suitability as a murine model of Duchenne muscular dystrophy. [PDF]
Various therapeutic approaches have been studied for the treatment of Duchenne muscular dystrophy (DMD), but none of these approaches have led to significant long-term effects in patients.
Kelly M Gutpell +2 more
doaj +1 more source
Sharing the load: compensatory pressure generation in the mdx mouse model. [PDF]
Khurram OU.
europepmc +3 more sources
Peptide-conjugated phosphodiamidate oligomer-mediated exon skipping has benefits for cardiac function in mdx and Cmah-/-mdx mouse models of Duchenne muscular dystrophy. [PDF]
Cardiac failure is a major cause of mortality in patients with Duchenne muscular dystrophy (DMD). Antisense-mediated exon skipping has the ability to correct out-of-frame mutations in DMD to produce truncated but functional dystrophin.
Alison M Blain +11 more
doaj +1 more source
Wild-type mouse models to screen antisense oligonucleotides for exon-skipping efficacy in Duchenne muscular dystrophy. [PDF]
A readily available animal model is essential for rapidly identifying effective treatments for Duchenne muscular dystrophy (DMD), a devastating neuromuscular disorder caused by the lack of dystrophin protein, which results from frame-disrupting mutations
Limin Cao, Gang Han, Ben Gu, HaiFang Yin
doaj +1 more source
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle weakness and wasting due to the lack of dystrophin protein. The acute phase of DMD is characterized by muscle necrosis and increased levels of the pro-inflammatory mediator ...
Sai Yarlagadda +3 more
doaj +1 more source
Comparative study of mesenchymal stem cells from C57BL/10 and mdx mice
Background Human mesenchymal stem cells (MSCs) have been studied and applied extensively because of their ability to self-renew and differentiate into various cell types. Since most human diseases models are murine, mouse MSCs should have been studied in
Xu Yong-feng +10 more
doaj +1 more source
This study aimed to evaluate cardiac function in a young mouse model of Duchenne muscular dystrophy (mdx) using cardiac magnetic resonance imaging (MRI) with feature tracking and self-gated magnetic resonance cine imaging.
Junpei Ueda, Shigeyoshi Saito
doaj +1 more source
Antisense-mediated exon skipping for Duchenne muscular dystrophy (DMD) is currently tested in phase 3 clinical trials. The aim of this approach is to modulate splicing by skipping a specific exon to reframe disrupted dystrophin transcripts, allowing the ...
Christa L Tanganyika-de Winter +6 more
doaj +1 more source

