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Cited by 4Muscle Physiology and DisordersCongenital heart defects researchMicroRNA in disease regulation

MicroRNA-33 inhibition ameliorates muscular dystrophy by enhancing skeletal muscle regeneration

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Sowa, Naoya, Horie, Takahiro, Ide, Yuya, Baba, Osamu, Kora, Kengo, Yoshida, Takeshi, Nakamura, Yujiro, Matsumura, Shigenobu +25 more·2025·EMBO Molecular Medicine
DOI 10.1038/s44321-025-00273-9PMC PMC12340133
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Abstract

Muscular dystrophy is a group of diseases characterized by progressive weakness and degeneration of skeletal muscles, for which there is currently no cure. Here, we show that microRNA (miR)-33a/b play a crucial role in muscle regeneration. miR-33a was upregulated during myoblast differentiation and in skeletal muscles of mdx mice, a genetic model of Duchenne muscular dystrophy (DMD). miR-33a deficiency enhanced muscle regeneration response to cardiotoxin injury and attenuated muscle degeneration and fibrosis in mdx mice. Conversely, a humanized mouse model expressing miR-33a and miR-33b showed exacerbated muscle degeneration and fibrosis. Mechanistically, miR-33a/b inhibited satellite cell proliferation, leading to reduced muscle regeneration and increased fibrosis by targeting Cdk6 , Fst , and Abca1 . Local and systemic administration of anti-miRNA oligonucleotides targeting miR-33a/b ameliorated the dystrophic phenotype in mdx mice. Furthermore, miR-33b inhibition upregulated these target genes in myotubes differentiated from human induced pluripotent stem cells derived from a patient with DMD. These findings indicate that miR-33a/b are involved in muscle regeneration and their inhibition may represent a potential therapeutic strategy for muscular dystrophy.

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  • miR-33b knock-in mice show exacerbated muscle damage and reduced exercise tolerance.

    “In contrast, miR-33b knock-in mice show exacerbated muscle damage and reduced exercise tolerance.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [45]

    The Results section reports greater fibrosis and elevated serum CK, along with reduced exercise capacity, in miR-33b-KI/mdx mice compared with WT/mdx mice. The claim omits the mdx background: the same section says miR-33b-KI mice without mdx showed no apparent changes in muscle histology. (LLM, conf=0.89)

    Experimental — accuracy not yet measured

  • In muscle stem cells (satellite cells), miR-33a/b suppress the expression of genes crucial for muscle regeneration and maturation, such as CDK6, FST, and ABCA1.

    “In muscle stem cells, known as satellite cells, miR-33a/b suppress the expression of genes crucial for muscle regeneration and maturation, such as cyclin-dependent kinase 6 (CDK6), follistatin (FST), and ABCA1 45 , 46) .”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [45]

    The Discussion (page unavailable) says miR-33a/b target Cdk6, Fst, and Abca1 and inhibit satellite-cell proliferation, supporting the claim’s main point. It does not establish that expression of all three genes is suppressed specifically within satellite cells; the Discussion instead describes ABCA1’s effect on fibrosis as potentially distinct from an increase in stem cells. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • miR-33a/b is abundantly expressed in skeletal muscle tissues and is important for muscular regeneration.

    “Recently, miR-33a/b was found to be abundantly expressed in skeletal muscle tissues and to be important for muscular regeneration.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [45]

  • Administration of synthetic nucleic acids to inhibit miR-33a/b promotes muscle regeneration, suppresses tissue fibrosis, and improves muscle function.

    “The administration of synthetic nucleic acids to inhibit miR-33a/b promotes muscle regeneration, suppresses tissue fibrosis, and improves the muscle function.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [45]

  • miR-33a knockout mice show enhanced skeletal muscle regeneration, and when crossbred with Duchene muscular dystrophy model mice (mdx mice), they exhibit ameliorated muscle damage and increased exercise tolerance.

    “MiR-33a knockout mice show enhanced skeletal muscle regeneration, and when crossbred with Duchene muscular dystrophy model mice (mdx mice), they exhibit ameliorated muscle damage and increased exercise tolerance.”

    From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [45]

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Research works printed but not linked: 60

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Authors
Sowa, N., Horie, T., Ide, Y., Baba, O., Kora, K., Yoshida, T., Nakamura, Y., Matsumura, S., Matsushita, K., Imanaka, M., Zou, F., Kume, E., Kojima, H., Qian, Q., Kimura, K., Otsuka, R., Hara, N., Yamasaki, T., Otani, C., Tsujisaka, Y., Takaya, T., Nishimura, C., Watanabe, D., Hasegawa, K., Kotera, J., Oka, K., Fujita, R., Takemiya, A., Sasaki, T., Kasahara, Y., Obika, S., Kimura, T., & Ono, K.
Affiliations
  • Kyoto University (JP)
  • Osaka Metropolitan University (JP)
  • Shinshu University (JP)
  • Kyoto Medical Center (JP)
  • Tanabe Pharma Corporation (Japan) (JP)
  • National Institute of Biomedical Innovation, Health and Nutrition (JP)
  • The University of Osaka (JP)
Corresponding author
  • Horie, Takahiro
  • Ono, Koh
ORCID
Venue
EMBO Molecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2025-07-23
Volume
17
Issue
8
Pages
1902-1925
ISSN
  • 1757-4676 (ISSN-L)
  • 1757-4684
DOI
10.1038/s44321-025-00273-9
PMC
PMC12340133
OpenAlex
W4412580626
Cited by
4
References
68
Citations by year
2026: 2 · 2025: 2
FWCI
1.20
Type
journal article
Language
en
Open access
Licence
Locations
  • EMBO Molecular Medicine (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Kyoto University Research Information Repository (Kyoto University) (submittedVersion, public-domain)
  • SOAR (Shinshu University) (submittedVersion, other-oa)
Funders
  • MEXT | Japan Society for the Promotion of Science (17K09860,20K08904,23K07988, 17H04177,20H03675,and 23K27595)
  • MEXT | JST | Fusion Oriented REsearch for disruptive Science and Technology (JPMJFR235F)
  • Japan Agency for Medical Research and Development (21ym0126013h0001,23ym0126074h0002, 24ek0210202h0001, 24am0521009)
  • Daiwa Securities Health Foundation
  • Takeda Science Foundation
  • Ono Medical Research Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Keywords
miR-33a, miR-33b, microRNA, muscular dystrophy, Duchenne muscular dystrophy, skeletal muscle regeneration, mdx mice, cardiotoxin injury, muscle fibrosis, satellite cell proliferation, CDK6, FST, ABCA1, antagomir, myogenesis, induced pluripotent stem cells, therapeutic target
MeSH terms
Animals, Cell Differentiation, Disease Models, Animal, Humans, Mice, Inbred C57BL, Regeneration, Mice, Inbred mdx, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Myoblasts, MicroRNAs, Cell Proliferation, Mice

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