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组蛋白 β-羟丁酸酰化在肌肉减少症的逆转中至关重要。

Histone β-hydroxybutyrylation is critical in reversal of sarcopenia.

机构信息

Metabolic Control and Aging, Human Aging Research Institute and School of Life Science, Nanchang University, and Jiangxi Key Laboratory of Aging and Diseases, Nanchang, China.

Institutional Center for Shared Technologies and Facilities of the Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.

出版信息

Aging Cell. 2024 Nov;23(11):e14284. doi: 10.1111/acel.14284. Epub 2024 Jul 30.

DOI:10.1111/acel.14284
PMID:39076122
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11561670/
Abstract

Sarcopenia, a leading cause for global disability and mortality, is an age-related muscular disorder, characterized by accelerated muscle mass loss and functional decline. It is known that caloric restriction (CR), ketogenic diet or endurance exercise lessen sarcopenia and elevate circulating β-hydroxybutyrate (β-HB) levels. Whether the elevated β-HB is essential to the reversal of sarcopenia, however, remains unclear. Here we show in both Caenorhabditis elegans and mouse models that an increase of β-HB reverse myofiber atrophy and improves motor functions at advanced ages. β-HB-induced histone lysine β-hydroxybutyrylation (Kbhb) is indispensable for the reversal of sarcopenia. Histone Kbhb enhances transcription of genes associated with mitochondrial pathways, including oxidative phosphorylation, ATP metabolic process and aerobic respiration. This ultimately leads to improve mitochondrial integrity and enhance mitochondrial respiration. The histone Kbhb are validated in mouse model with CR. Thus, we demonstrate that β-HB induces histone Kbhb, increases mitochondrial function, and reverses sarcopenia.

摘要

肌肉减少症是全球残疾和死亡的主要原因，是一种与年龄相关的肌肉疾病，其特征是肌肉质量迅速丧失和功能下降。众所周知，热量限制（CR）、生酮饮食或耐力运动可以减轻肌肉减少症并提高循环β-羟基丁酸（β-HB）水平。然而，升高的β-HB 是否对肌肉减少症的逆转至关重要尚不清楚。在这里，我们在秀丽隐杆线虫和小鼠模型中均表明，β-HB 的增加可逆转肌纤维萎缩并改善高龄动物的运动功能。β-HB 诱导的组蛋白赖氨酸β-羟丁酰化（Kbhb）对于肌肉减少症的逆转是必不可少的。组蛋白 Kbhb 增强了与线粒体途径相关的基因的转录，包括氧化磷酸化、ATP 代谢过程和需氧呼吸。这最终导致改善线粒体完整性并增强线粒体呼吸。CR 小鼠模型中验证了组蛋白 Kbhb。因此，我们证明β-HB 诱导组蛋白 Kbhb，增加线粒体功能，并逆转肌肉减少症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/48edef3bdcfe/ACEL-23-e14284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/24e8b2e78b08/ACEL-23-e14284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/81d3bfaf37aa/ACEL-23-e14284-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/09f28a0af3cd/ACEL-23-e14284-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/53fd27934800/ACEL-23-e14284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/87d3d0251d15/ACEL-23-e14284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/48edef3bdcfe/ACEL-23-e14284-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/24e8b2e78b08/ACEL-23-e14284-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/81d3bfaf37aa/ACEL-23-e14284-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/09f28a0af3cd/ACEL-23-e14284-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/53fd27934800/ACEL-23-e14284-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/87d3d0251d15/ACEL-23-e14284-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1255/11561670/48edef3bdcfe/ACEL-23-e14284-g001.jpg

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