Molecular and Cellular Exercise Physiology, Department of Physiology and Pharmacology, Biomedicum, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093.
Proc Natl Acad Sci U S A. 2024 Aug 20;121(34):e2319724121. doi: 10.1073/pnas.2319724121. Epub 2024 Aug 14.
Skeletal muscle atrophy is a morbidity and mortality risk factor that happens with disuse, chronic disease, and aging. The tissue remodeling that happens during recovery from atrophy or injury involves changes in different cell types such as muscle fibers, and satellite and immune cells. Here, we show that the previously uncharacterized gene and protein Zfp697 is a damage-induced regulator of muscle remodeling. Zfp697/ZNF697 expression is transiently elevated during recovery from muscle atrophy or injury in mice and humans. Sustained Zfp697 expression in mouse muscle leads to a gene expression signature of chemokine secretion, immune cell recruitment, and extracellular matrix remodeling. Notably, although Zfp697 is expressed in several cell types in skeletal muscle, myofiber-specific Zfp697 genetic ablation in mice is sufficient to hinder the inflammatory and regenerative response to muscle injury, compromising functional recovery. We show that Zfp697 is an essential mediator of the interferon gamma response in muscle cells and that it functions primarily as an RNA-interacting protein, with a very high number of miRNA targets. This work identifies Zfp697 as an integrator of cell-cell communication necessary for tissue remodeling and regeneration.
骨骼肌萎缩是一种发病率和死亡率的风险因素,与废用、慢性疾病和衰老有关。在从萎缩或损伤中恢复的过程中发生的组织重塑涉及到不同细胞类型的变化,如肌肉纤维、卫星细胞和免疫细胞。在这里,我们表明,以前未被描述的基因和蛋白质 Zfp697 是肌肉重塑的损伤诱导调节剂。Zfp697/ZNF697 的表达在小鼠和人类从肌肉萎缩或损伤中恢复时会短暂升高。在小鼠肌肉中持续表达 Zfp697 会导致趋化因子分泌、免疫细胞募集和细胞外基质重塑的基因表达特征。值得注意的是,尽管 Zfp697 在骨骼肌中的几种细胞类型中表达,但在小鼠中特异性敲除肌纤维中的 Zfp697 足以阻碍肌肉损伤的炎症和再生反应,从而影响功能恢复。我们表明,Zfp697 是肌肉细胞中干扰素 γ反应的必需介质,它主要作为一种 RNA 相互作用蛋白发挥作用,具有非常多的 miRNA 靶标。这项工作确定了 Zfp697 作为细胞间通讯的整合因子,对于组织重塑和再生是必要的。