Inhibition of myostatin in adult mice increases skeletal muscle mass and strength

Whittemore, Lisa-Anne; Song, Kening; Li, Xiangping; Aghajanian, J. D.; Davies, Monique V.; Girgenrath, Stefan; Hill, Jonathan D.; Jalenak, Mary; Kelley, Pamela; Knight, Andrea; Maylor, Rich; O’Hara, Denise M; Pearson, Adele A.; Quazi, Amira; Ryerson, Stephanie; Tan, Xiang Yang; Tomkinson, Kathleen; Veldman, Geertruida M.; Widom, Angela; Wright, Jill F.; Wudyka, Steve; Zhao, Liz; Wolfman, Neil M.

doi:10.1016/s0006-291x(02)02953-4

Cited by 441 publications

(377 citation statements)

References 30 publications

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“…An anti-myostatin antibody (JA16) has been shown to increase muscle mass in healthy adult mice. 8 In the present study, we focused on the use of in vivo systems and showed that antisense RNA oligonucleotides could downregulate the target gene myostatin expression in vivo, leading to an increase of the muscle weight in normal mice. Our results further strengthen the notion that myostatin is an important therapeutic target for muscle wasting-related conditions.…”

Section: Discussionmentioning

confidence: 93%

Myostatin antisense RNA-mediated muscle growth in normal and cancer cachexia mice

Yang

Liu

et al. 2007

Gene Ther

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Myostatin is a negative regulator of myogenesis, and inactivation of myostatin leads to muscle growth. Here we have used modified RNA oligonucleotides targeting the myostatin mRNA and examined the therapeutic potential in normal and cancer cachexia mouse models. We found that the RNA oligonucleotides could suppress the myostatin expression in vivo, leading to the increase in muscle growth both in normal and cachectic mice. We also established that the effect of myostatin inhibition caused by the RNA oligonucleotides may be through the MyoD pathway, as evidenced by a significant upregulation of MyoD expression. Taken together, these results demonstrate the feasibility using antisense strategy for the treatment of muscle wasting conditions. Gene Therapy (2008) 15, 155-160;

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Section: Discussionmentioning

confidence: 93%

Myostatin antisense RNA-mediated muscle growth in normal and cancer cachexia mice

Yang

Liu

et al. 2007

Gene Ther

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“…In skeletal muscle, myostatin inhibits muscle cell growth and differentiation, 54,55 and myostatin knockout mice have an increased muscle mass and decreased fat mass. 56 Interestingly, these knockout mice have a dramatic increase in beiging of scWAT. 51 Incubation of cells cultured from the stromal vascular fraction of scWAT and incubated with media conditioned with skeletal muscle from myostatin knockout mice resulted in a marked beiging of the SVF cells.…”

Section: Myostatinmentioning

confidence: 99%

Exercise regulation of adipose tissue

2016

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Exercise training results in adaptations to numerous organ systems and offers protection against metabolic disorders including obesity and type 2 diabetes, and recent reports suggest that adipose tissue may play a role in these beneficial effects of exercise on overall health. Multiple studies have investigated the effects of exercise training on both white adipose tissue (WAT) and brown adipose tissue (BAT), as well as the induction of beige adipocytes. Studies from both rodents and humans show that there are exercise training-induced changes in WAT including decreased cell size and lipid content, and increased mitochondrial activity. In rodents, exercise training causes an increased beiging of WAT. Whether exercise training causes a beiging of human scWAT, as well as which factors contribute to the exercise-induced beiging of WAT are areas of current investigation. Studies investigating the effects of exercise training on BAT mass and function have yielded conflicting data, and hence, is another area of intensive investigation. This review will focus on studies aimed at elucidating the mechanisms regulating exercise training induced-adaptations to adipose tissue.

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“…Moreover, inhibition of this endocrine function results in muscle hypertrophy in mice (Whittemore et al. 2003). …”

Section: Introductionmentioning

confidence: 99%

Lifelong exercise, but not short-term high-intensity interval training, increases GDF11, a marker of successful aging: a preliminary investigation

et al. 2017

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Lifelong exercise is associated with regulation of skeletal mass and function, reductions in frailty, and successful aging. Yet, the influence of exercise on myostatin and myostatin‐interacting factors is relatively under examined in older males. Therefore, we investigated whether serum total myostatin, free myostatin, follistatin, and growth and differentiation factor 11 (GDF11) were altered following high‐intensity interval training (HIIT) in a group of 13 lifelong sedentary (SED; 64 [6] years) and 11 lifelong exercising (LEX; 62 [6] years) older males. SED follistatin was moderately greater than LEX pre‐HIIT (Cohen's d = 0.66), and was largely greater post‐HIIT (Cohen's d = 1.22). The HIIT‐induced increase in follistatin was large in SED (Cohen's d = 0.82) and absent in LEX (Cohen's d = 0.03). GDF11 was higher in LEX pre‐HIIT (Cohen's d = 0.49) and post‐HIIT (Cohen's d = 0.63) compared to SED. HIIT resulted in no change to GDF11 in LEX or SED (Cohen's d = 0.00–0.03). Peak power output and GDF11 were correlated (r = 0.603), independent of grouping. Differences in GDF11 with lifelong exercise training, paired with the correlation between GDF11 and peak power output, suggested that GDF11 may be a relevant myostatin‐interacting peptide to successful aging in humans, and strategies to maintain this need to be further explored.

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Inhibition of myostatin in adult mice increases skeletal muscle mass and strength

Cited by 441 publications

References 30 publications

Myostatin antisense RNA-mediated muscle growth in normal and cancer cachexia mice

Myostatin antisense RNA-mediated muscle growth in normal and cancer cachexia mice

Exercise regulation of adipose tissue

Lifelong exercise, but not short-term high-intensity interval training, increases GDF11, a marker of successful aging: a preliminary investigation

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