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缺乏证据表明生长分化因子11是老年骨骼肌卫星细胞的年轻化因子。

Lack of evidence for GDF11 as a rejuvenator of aged skeletal muscle satellite cells.

作者信息

Hinken Aaron C, Powers Janine M, Luo Guizhen, Holt Jason A, Billin Andrew N, Russell Alan J

机构信息

GlaxoSmithKline, Muscle Metabolism Discovery Performance Unit, 709 Swedeland Road, King of Prussia, PA, 19406, USA.

Five Prime Therapeutics, Two Corporate Drive, South San Francisco, CA, 94080, USA.

出版信息

Aging Cell. 2016 Jun;15(3):582-4. doi: 10.1111/acel.12475. Epub 2016 Mar 28.

DOI:10.1111/acel.12475
PMID:27139744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4854912/
Abstract

Recent high-profile studies report GDF11 to be a key circulating 'anti-aging' factor. However, a screen of extracellular proteins attempting to identify factors with 'anti-aging' phenotypes in aged murine skeletal muscle satellite cells did not identify GDF11 activity. We have been unable to confirm the reported activity of GDF11, similar to other laboratories offering conflicting data and describe our attempts to do so in this short take.

摘要

近期备受瞩目的研究报告称生长分化因子11（GDF11）是一种关键的循环“抗衰老”因子。然而，一项针对细胞外蛋白质的筛选，旨在鉴定老年小鼠骨骼肌卫星细胞中具有“抗衰老”表型的因子，却未发现GDF11的活性。我们无法证实GDF11所报道的活性，其他实验室也提供了相互矛盾的数据，在此简短报告中我们描述了为此所做的尝试。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f3/4854912/26f8db780db6/ACEL-15-582-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f3/4854912/26f8db780db6/ACEL-15-582-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3f3/4854912/26f8db780db6/ACEL-15-582-g001.jpg

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Deorphanization of the human leukocyte tyrosine kinase (LTK) receptor by a signaling screen of the extracellular proteome.
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循环 GDF11 可加重小鼠心肌损伤，并与人类心肌梗死面积增大相关。
Cardiovasc Res. 2023 Dec 30;119(17):2729-2742. doi: 10.1093/cvr/cvad153.
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