Maintenance of type 2 glycolytic myofibers with age by Mib1-Actn3 axis

Ji-Yun Seo, Jong-Seol Kang, Ye Lynne Kim, Young-Woo Jo, Ji-Hoon Kim, Sang-Hyeon Hann, Jieon Park, Inkuk Park, Hyerim Park, Kyusang Yoo, Joonwoo Rhee, Jung-Wee Park, Yong Chan Ha and Young-Yun Kong ()
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Ji-Yun Seo: Seoul National University
Jong-Seol Kang: Seoul National University
Ye Lynne Kim: Seoul National University
Young-Woo Jo: Seoul National University
Ji-Hoon Kim: Seoul National University
Sang-Hyeon Hann: Seoul National University
Jieon Park: Seoul National University
Inkuk Park: Seoul National University
Hyerim Park: Seoul National University
Kyusang Yoo: Seoul National University
Joonwoo Rhee: Seoul National University
Jung-Wee Park: Chung-Ang University College of Medicine
Yong Chan Ha: Chung-Ang University College of Medicine
Young-Yun Kong: Seoul National University

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Age-associated muscle atrophy is a debilitating condition associated with loss of muscle mass and function with age that contributes to limitation of mobility and locomotion. However, the underlying mechanisms of how intrinsic muscle changes with age are largely unknown. Here we report that, with age, Mind bomb-1 (Mib1) plays important role in skeletal muscle maintenance via proteasomal degradation-dependent regulation of α-actinin 3 (Actn3). The disruption of Mib1 in myofibers (Mib1ΔMF) results in alteration of type 2 glycolytic myofibers, muscle atrophy, impaired muscle function, and Actn3 accumulation. After chronic exercise, Mib1ΔMF mice show muscle atrophy even at young age. However, when Actn3 level is downregulated, chronic exercise-induced muscle atrophy is ameliorated. Importantly, the Mib1 and Actn3 levels show clinical relevance in human skeletal muscles accompanied by decrease in skeletal muscle function with age. Together, these findings reveal the significance of the Mib1-Actn3 axis in skeletal muscle maintenance with age and suggest the therapeutic potential for the treatment or amelioration of age-related muscle atrophy.

Date: 2021
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DOI: 10.1038/s41467-021-21621-6

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