Becker muscular dystrophy mice showed site-specific decay of type IIa fibers with capillary change in skeletal muscle Article Swipe
Daigo Miyazaki
,
Mitsuto Sato
,
Naoko Shiba
,
Takahiro Yoshizawa
,
Akinori Nakamura
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.7554/elife.100665.1
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.7554/elife.100665.1
Becker muscular dystrophy (BMD), an X-linked muscular dystrophy, is mostly caused by an in-frame deletion of DMD. BMD severity varies from asymptomatic to severe, associated with the genotype of DMD. However, the underlying mechanisms remain unclear. We established BMD mice carrying three representative exon deletions: ex45–48 del., ex45–47 del., and ex45–49 del. (d45–48, d45–47 and d45–49), with high frequencies and different severities in the human BMD hotspot. All three BMD mice showed muscle weakness, muscle degeneration, and fibrosis, but these changes appeared at different times for each exon deletion, consistent with the severities obtained by the natural history study of BMD. BMD mice showed site-specific muscle changes, unlike mdx mice, which showed diffuse muscle changes, and we demonstrated selective type IIa fiber reduction in BMD mice. Furthermore, BMD mice showed sarcolemmal neuronal nitric oxide synthetase (nNOS) reduction and morphological capillary changes around type IIa fibers. These results suggest that capillary changes caused by nNOS reduction may be associated with the mechanism of skeletal muscle degeneration and type IIa fiber reduction in BMD mice. BMD mice may be useful in elucidating the pathomechanisms and developing therapeutic strategies for human BMD.
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- preprint
- Language
- en
- Landing Page
- https://doi.org/10.7554/elife.100665.1
- OA Status
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- References
- 48
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https://doi.org/10.7554/elife.100665.1Digital Object Identifier
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Becker muscular dystrophy mice showed site-specific decay of type IIa fibers with capillary change in skeletal muscleWork title
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
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2024-10-23Full publication date if available
- Authors
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Daigo Miyazaki, Mitsuto Sato, Naoko Shiba, Takahiro Yoshizawa, Akinori NakamuraList of authors in order
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https://doi.org/10.7554/elife.100665.1Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.7554/elife.100665.1Direct OA link when available
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Muscular dystrophy, Skeletal Muscle Fibers, Capillary action, Skeletal muscle, Anatomy, Chemistry, Medicine, Materials science, Internal medicine, Composite materialTop concepts (fields/topics) attached by OpenAlex
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0Total citation count in OpenAlex
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48Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.which | 111 |
| abstract_inverted_index.(BMD), | 4 |
| abstract_inverted_index.(nNOS) | 136 |
| abstract_inverted_index.Becker | 1 |
| abstract_inverted_index.around | 142 |
| abstract_inverted_index.caused | 11, 152 |
| abstract_inverted_index.mostly | 10 |
| abstract_inverted_index.muscle | 73, 75, 106, 114, 164 |
| abstract_inverted_index.nitric | 133 |
| abstract_inverted_index.remain | 35 |
| abstract_inverted_index.showed | 72, 104, 112, 130 |
| abstract_inverted_index.unlike | 108 |
| abstract_inverted_index.useful | 178 |
| abstract_inverted_index.varies | 20 |
| abstract_inverted_index.changes | 81, 141, 151 |
| abstract_inverted_index.diffuse | 113 |
| abstract_inverted_index.fibers. | 145 |
| abstract_inverted_index.history | 98 |
| abstract_inverted_index.natural | 97 |
| abstract_inverted_index.results | 147 |
| abstract_inverted_index.severe, | 24 |
| abstract_inverted_index.suggest | 148 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.However, | 31 |
| abstract_inverted_index.X-linked | 6 |
| abstract_inverted_index.appeared | 82 |
| abstract_inverted_index.carrying | 41 |
| abstract_inverted_index.changes, | 107, 115 |
| abstract_inverted_index.d45–47 | 54 |
| abstract_inverted_index.deletion | 15 |
| abstract_inverted_index.genotype | 28 |
| abstract_inverted_index.hotspot. | 67 |
| abstract_inverted_index.in-frame | 14 |
| abstract_inverted_index.muscular | 2, 7 |
| abstract_inverted_index.neuronal | 132 |
| abstract_inverted_index.obtained | 94 |
| abstract_inverted_index.severity | 19 |
| abstract_inverted_index.skeletal | 163 |
| abstract_inverted_index.unclear. | 36 |
| abstract_inverted_index.capillary | 140, 150 |
| abstract_inverted_index.deletion, | 89 |
| abstract_inverted_index.different | 61, 84 |
| abstract_inverted_index.dystrophy | 3 |
| abstract_inverted_index.ex45–47 | 48 |
| abstract_inverted_index.ex45–48 | 46 |
| abstract_inverted_index.ex45–49 | 51 |
| abstract_inverted_index.fibrosis, | 78 |
| abstract_inverted_index.mechanism | 161 |
| abstract_inverted_index.reduction | 123, 137, 155, 170 |
| abstract_inverted_index.selective | 119 |
| abstract_inverted_index.weakness, | 74 |
| abstract_inverted_index.(d45–48, | 53 |
| abstract_inverted_index.associated | 25, 158 |
| abstract_inverted_index.consistent | 90 |
| abstract_inverted_index.d45–49), | 56 |
| abstract_inverted_index.deletions: | 45 |
| abstract_inverted_index.developing | 184 |
| abstract_inverted_index.dystrophy, | 8 |
| abstract_inverted_index.mechanisms | 34 |
| abstract_inverted_index.severities | 62, 93 |
| abstract_inverted_index.strategies | 186 |
| abstract_inverted_index.synthetase | 135 |
| abstract_inverted_index.underlying | 33 |
| abstract_inverted_index.elucidating | 180 |
| abstract_inverted_index.established | 38 |
| abstract_inverted_index.frequencies | 59 |
| abstract_inverted_index.sarcolemmal | 131 |
| abstract_inverted_index.therapeutic | 185 |
| abstract_inverted_index.Furthermore, | 127 |
| abstract_inverted_index.asymptomatic | 22 |
| abstract_inverted_index.degeneration | 165 |
| abstract_inverted_index.demonstrated | 118 |
| abstract_inverted_index.degeneration, | 76 |
| abstract_inverted_index.morphological | 139 |
| abstract_inverted_index.site-specific | 105 |
| abstract_inverted_index.representative | 43 |
| abstract_inverted_index.pathomechanisms | 182 |
| cited_by_percentile_year | |
| countries_distinct_count | 1 |
| institutions_distinct_count | 5 |
| citation_normalized_percentile.value | 0.20910069 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |