Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY, 14642, USA.
Clinical and Translational Science Institute, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY, 14642, USA.
Arch Toxicol. 2024 Jun;98(6):1645-1658. doi: 10.1007/s00204-024-03724-3. Epub 2024 Mar 28.
A number of environmental toxicants are noted for their activity that leads to declined motor function. However, the role of muscle as a proximal toxicity target organ for environmental agents has received considerably less attention than the toxicity targets in the nervous system. Nonetheless, the effects of conventional neurotoxicants on processes of myogenesis and muscle maintenance are beginning to resolve a concerted role of muscle as a susceptible toxicity target. A large body of evidence from epidemiological, animal, and in vitro studies has established that methylmercury (MeHg) is a potent developmental toxicant, with the nervous system being a preferred target. Despite its well-recognized status as a neurotoxicant, there is accumulating evidence that MeHg also targets muscle and neuromuscular development as well as contributes to the etiology of motor defects with prenatal MeHg exposure. Here, we summarize evidence for targets of MeHg in the morphogenesis and maintenance of skeletal muscle that reveal effects on MeHg distribution, myogenesis, myotube formation, myotendinous junction formation, neuromuscular junction formation, and satellite cell-mediated muscle repair. We briefly recapitulate the molecular and cellular mechanisms of skeletal muscle development and highlight the pragmatic role of alternative model organisms, Drosophila and zebrafish, in delineating the molecular underpinnings of muscle development and MeHg-mediated myotoxicity. Finally, we discuss how toxicity targets in muscle development may inform the developmental origins of health and disease theory to explain the etiology of environmentally induced adult motor deficits and accelerated decline in muscle fitness with aging.
许多环境毒物因其导致运动功能下降的活性而受到关注。然而,肌肉作为环境剂的近端毒性靶器官的作用,受到的关注远远少于神经系统的毒性靶标。尽管如此,传统神经毒物对成肌过程和肌肉维持的影响,开始确定肌肉作为易受毒性靶标的协同作用。大量来自流行病学、动物和体外研究的证据已经证实,甲基汞(MeHg)是一种有效的发育毒物,神经系统是首选靶标。尽管它作为神经毒物的地位得到了很好的认可,但越来越多的证据表明,MeHg 还针对肌肉和神经肌肉发育,并导致产前 MeHg 暴露引起的运动缺陷的病因。在这里,我们总结了 MeHg 在骨骼肌肉形态发生和维持中的靶标证据,这些证据揭示了 MeHg 分布、成肌、肌管形成、肌腱连接形成、神经肌肉连接形成和卫星细胞介导的肌肉修复等方面的影响。我们简要回顾了骨骼肌发育的分子和细胞机制,并强调了替代模式生物果蝇和斑马鱼在阐明肌肉发育和 MeHg 介导的肌毒性的分子基础方面的实际作用。最后,我们讨论了肌肉发育中的毒性靶标如何为健康和疾病的发育起源理论提供信息,以解释环境诱导的成年运动缺陷的病因和衰老过程中肌肉功能的加速衰退。