ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Loss of ARNT in skeletal muscle limits muscle regeneration in aging.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Article
- Inhibition of p53-MDM2 binding reduces senescent cell abundance and improves the adaptive responses of skeletal muscle from aged mice.GeroScience · 2024Article
- VEGFA Promotes Skeletal Muscle Regeneration in Aging.Advanced biology · 2023Article
- Maladaptive Immune Activation in Age-Related Decline of Muscle Function.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Review
- Aerobic exercise and scaffolds with hierarchical porosity synergistically promote functional recovery post volumetric muscle loss.Biomaterials · 2023Article
- Article
- Deletion of SA β-Gal+ cells using senolytics improves muscle regeneration in old mice.Aging cell · 2022Article
- Muscle Cryoinjury and Quantification of Regenerating Myofibers in Mice.Bio-protocol · 2021Article
- Loss of ARNT in skeletal muscle limits muscle regeneration in aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
The ability of skeletal muscle to regenerate declines significantly with aging. The expression of aryl hydrocarbon receptor nuclear translocator (ARNT), a critical component of the hypoxia signaling pathway, was less abundant in skeletal muscle of old (23-25 months old) mice. This loss of ARNT was associated with decreased levels of Notch1 intracellular domain (N1ICD) and impaired regenerative response to injury in comparison to young (2-3 months old) mice. Knockdown of ARNT in a primary muscle cell line impaired differentiation in vitro. Skeletal muscle-specific ARNT deletion in young mice resulted in decreased levels of whole muscle N1ICD and limited muscle regeneration. Administration of a systemic hypoxia pathway activator (ML228), which simulates the actions of ARNT, rescued skeletal muscle regeneration in both old and ARNT-deleted mice. These results suggest that the loss of ARNT in skeletal muscle is partially responsible for diminished myogenic potential in aging and activation of hypoxia signaling holds promise for rescuing regenerative activity in old muscle.
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