Sone Masamitsu, Yamaguchi Yoshifumi
Hibernation Metabolism, Physiology and Development Group, Institute of Low Temperature Science, Hokkaido University, Sapporo, Japan.
Graduate School of Environmental Science, Hokkaido University, Sapporo, Japan.
Front Physiol. 2024 Apr 25;15:1377986. doi: 10.3389/fphys.2024.1377986. eCollection 2024.
Most mammals adapt thermal physiology around 37°C and large deviations from their range, as observed in severe hypothermia and hyperthermia, resulting in organ dysfunction and individual death. A prominent exception is mammalian hibernation. Mammalian hibernators resist the long-term duration of severe low body temperature that is lethal to non-hibernators, including humans and mice. This cold resistance is supported, at least in part, by intrinsic cellular properties, since primary or immortalized cells from several hibernator species can survive longer than those from non-hibernators when cultured at cold temperatures. Recent studies have suggested that cold-induced cell death fulfills the hallmarks of ferroptosis, a type of necrotic cell death that accompanies extensive lipid peroxidation by iron-ion-mediated reactions. In this review, we summarize the current knowledge of cold resistance of mammalian hibernators at the cellular and molecular levels to organ and systemic levels and discuss key pathways that confer cold resistance in mammals.
大多数哺乳动物将热生理调节至37°C左右,而严重体温过低和体温过高时出现的与其范围的大幅偏差会导致器官功能障碍和个体死亡。一个显著的例外是哺乳动物的冬眠。哺乳动物冬眠者能抵御对非冬眠者(包括人类和小鼠)致命的长期严重低温。这种抗寒能力至少部分由内在细胞特性支撑,因为在低温培养时,来自几种冬眠动物物种的原代或永生化细胞比来自非冬眠动物的细胞存活时间更长。最近的研究表明,冷诱导的细胞死亡符合铁死亡的特征,铁死亡是一种坏死性细胞死亡,伴随着铁离子介导的反应导致广泛的脂质过氧化。在这篇综述中,我们总结了目前关于哺乳动物冬眠者在细胞和分子水平至器官和系统水平的抗寒知识,并讨论了赋予哺乳动物抗寒能力的关键途径。