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首页> 外文期刊>Cell metabolism >GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration
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GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration

机译：GDF11随着年龄的增长而增加，并抑制骨骼肌再生

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摘要

Age-related frailty may be due to decreased skeletal muscle regeneration. The role of TGF-beta molecules myostatin and GDF11 in regeneration is unclear. Recent studies showed an age-related decrease in GDF11 and that GDF11 treatment improves muscle regeneration, which were contrary to prior studies. We now show that these recent claims are not reproducible and the reagents previously used to detect GDF11 are not GDF11 specific. We develop a GDF11-specific immunoassay and show a trend toward increased GDF11 levels in sera of aged rats and humans. GDF11 mRNA increases in rat muscle with age. Mechanistically, GDF11 and myostatin both induce SMAD2/3 phosphorylation, inhibit myoblast differentiation, and regulate identical downstream signaling. GDF11 significantly inhibited muscle regeneration and decreased satellite cell expansion in mice. Given early data in humans showing a trend for an age-related increase, GDF11 could be a target for pharmacologic blockade to treat age-related sarcopenia.
机译：与年龄有关的虚弱可能是由于骨骼肌再生减少。 TGF-β分子肌生长抑制素和GDF11在再生中的作用尚不清楚。最近的研究表明，与年龄相关的GDF11下降和GDF11治疗可改善肌肉再生，这与先前的研究相反。我们现在显示这些最近的权利要求是不可再现的，以前用于检测GDF11的试剂不是GDF11特异性的。我们开发了GDF11特异性免疫测定法，并显示了老年大鼠和人类血清中GDF11水平升高的趋势。 GDF11 mRNA在大鼠肌肉中随年龄增长而增加。从机制上讲，GDF11和肌生长抑制素都诱导SMAD2 / 3磷酸化，抑制成肌细胞分化，并调节相同的下游信号传导。 GDF11显着抑制小鼠的肌肉再生并减少卫星细胞的扩张。鉴于人类的早期数据显示出与年龄相关的增加趋势，GDF11可能成为治疗与年龄相关的肌肉减少症的药理障碍的靶标。

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