15 April 2024 | Veronika R. Kedlian, Yaning Wang, Tianliang Liu, Xiaoping Chen, Liam Bolt, Catherine Tudor, Zhuojian Shen, Eirini S. Fasouli, Elena Prigmore, Vitalii Kleshchevnikov, Jan Patrick Pett, Tong Li, John E. G. Lawrence, Shani Perera, Martin Prete, Ni Huang, Qin Guo, Xinrui Zeng, Lu Yang, Krzysztof Polański, Nana-Jane Chipampe, Monika Dabrowska, Xiaoao Li, Omer Ali Bayraktar, Minal Patel, Natsuhiko Kumasaka, Krishnaa T. Mahbubani, Andy Peng Xiang, Kerstin B. Meyer, Kourosh Saeb-Parsy, Sarah A. Teichmann, Hongbo Zhang
This study profiles the aging process in adult human intercostal muscle by analyzing 90,902 single cells and 92,259 single nuclei from 17 donors. The researchers identified distinct subsets of muscle stem cells (MuSCs) with decreased ribosome biogenesis genes and increased CCL2 expression, leading to different aging phenotypes. The atlas also highlights an expansion of nuclei associated with the neuromuscular junction, which may reflect re-innervation, and outlines how the loss of fast-twitch myofibers is mitigated through regeneration and upregulation of fast-type markers in slow-twitch myofibers. Additionally, the study documents the function of the aging muscle microenvironment in immune cell attraction. The comprehensive human skeletal muscle aging resource is available at <https://www.muscleagingcellatlas.org/>, and an in-house mouse muscle atlas is provided to study common features of muscle aging across species. Key findings include the identification of aging mechanisms acting in parallel across different cell compartments, such as decreased MuSC activation and increased pro-inflammatory pathways, and the observation of compensatory changes in response to the loss of fast-twitch myofibers. The study also describes a previously unreported type of neuromuscular junction accessory population that may contribute to re-innervation.This study profiles the aging process in adult human intercostal muscle by analyzing 90,902 single cells and 92,259 single nuclei from 17 donors. The researchers identified distinct subsets of muscle stem cells (MuSCs) with decreased ribosome biogenesis genes and increased CCL2 expression, leading to different aging phenotypes. The atlas also highlights an expansion of nuclei associated with the neuromuscular junction, which may reflect re-innervation, and outlines how the loss of fast-twitch myofibers is mitigated through regeneration and upregulation of fast-type markers in slow-twitch myofibers. Additionally, the study documents the function of the aging muscle microenvironment in immune cell attraction. The comprehensive human skeletal muscle aging resource is available at <https://www.muscleagingcellatlas.org/>, and an in-house mouse muscle atlas is provided to study common features of muscle aging across species. Key findings include the identification of aging mechanisms acting in parallel across different cell compartments, such as decreased MuSC activation and increased pro-inflammatory pathways, and the observation of compensatory changes in response to the loss of fast-twitch myofibers. The study also describes a previously unreported type of neuromuscular junction accessory population that may contribute to re-innervation.