神经鞘瘤是由施万细胞（SC）转化引起的周围神经系统良性肿瘤。总体而言，这些肿瘤与神经纤维蛋白 2 型基因的改变有关，该基因编码肿瘤抑制蛋白 merlin，这是一种属于埃兹蛋白-根蛋白-莫斯蛋白家族的细胞骨架相关蛋白。然而，神经鞘瘤发病和进展的潜在机制尚未完全阐明，而挑战之一可能是环境。有鉴于此，尽管证据主要是流行病学的，但暴露于使用普通电气设备产生的电磁场（EMF）已被挑衅地认为是 SC 转化的原因。事实上，迄今为止，尚未确定解释 SC 肿瘤转化的非实质性机制。最近，一些体外证据指出暴露于 EMF（0.1 T，50 Hz，10 min）的 SC 的增殖和迁移能力发生变化。在这里，我们使用相同的实验范式来讨论 SCs 适应 EMF 中假定的表观遗传机制的参与，并解释暴露后缺氧变化的发生。我们的研究结果表明，SC 发生了一系列环境诱导的变化，趋向于较不生理的状态，这可能与 SC 分化和神经鞘瘤发展具有病理相关性。© 2024 Wiley periodicals LLC。

Schwannomas are benign tumors of the peripheral nervous system arising from the transformation of Schwann cells (SCs). On the whole, these tumors are related to alterations of the neurofibromin type 2 gene, coding for the oncosuppressor merlin, a cytoskeleton-associated protein belonging to the ezrin-radixin-moesin family. However, the underlying mechanisms of schwannoma onset and progression are not fully elucidated, whereas one of the challenges might be the environment. In this light, the exposure to electromagnetic field (EMF), generated by the use of common electrical devices, has been defiantly suggested as the cause of SCs transformation even if the evidence was mostly epidemiologic. Indeed, insubstantial mechanisms have been so far identified to explain SCs oncotransformation. Recently, some in vitro evidence pointed out alterations in proliferation and migration abilities in SCs exposed to EMF (0.1 T, 50 Hz, 10 min). Here, we used the same experimental paradigma to discuss the involvement of putative epigenetic mechanisms in SCs adaptation to EMF and to explain the occurrence of hypoxic alterations after the exposure. Our findings indicate a set of environmental-induced changes in SCs, toward a less-physiological state, which may be pathologically relevant for the SCs differentiation and the schwannoma development.© 2024 Wiley Periodicals LLC.