Zhu Zhen, Wu Jiang, Wen Yuguo, Wu Xiaocheng, Bao Huimingda, Wang Min, Kang Kai
Department of Animal Science, College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang 524088, China.
Department of Veterinary Medicine, College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang 524088, China.
Vet Sci. 2024 Oct 1;11(10):464. doi: 10.3390/vetsci11100464.
Heat stress has been one of the key research areas for researchers due to the wide-ranging effects and complex mechanisms of action of its stress product reactive oxygen species (ROS). The aim of this paper is to comprehensively review and summarize the effects of heat stress on ovarian granulosa cells and their mechanism of action. We systematically reviewed the effects of heat stress on ovarian granulosa cells, including intracellular steroid hormone changes, oxidative stress, apoptosis, and mitochondrial function. Meanwhile, this paper discusses in detail several major mechanisms by which heat stress induces apoptosis in ovarian granulosa cells, such as through the activation of apoptosis-related genes, induction of endoplasmic reticulum stress, and the mitochondrial pathway. In addition, we analyzed the mechanism of ferroptosis in ovarian granulosa cells under heat stress conditions, summarized the potential association between heat stress and ferroptosis in light of the existing literature, and explored the key factors in the mechanism of action of heat stress, such as the signaling pathways of Nrf2/Keap1, HSPs, and JNK, and analyzed their possible roles in the process of ferroptosis. Finally, this paper provides an outlook on the future research direction, describing the possible interaction between heat stress and ferroptosis, with a view to providing a theoretical basis for further understanding and revealing the complex mechanism of ferroptosis occurrence in ovarian granulosa cells under heat stress.
由于热应激产物活性氧(ROS)具有广泛的影响和复杂的作用机制,热应激一直是研究人员的关键研究领域之一。本文旨在全面综述和总结热应激对卵巢颗粒细胞的影响及其作用机制。我们系统地回顾了热应激对卵巢颗粒细胞的影响,包括细胞内甾体激素变化、氧化应激、细胞凋亡和线粒体功能。同时,本文详细讨论了热应激诱导卵巢颗粒细胞凋亡的几种主要机制,如通过激活凋亡相关基因、诱导内质网应激和线粒体途径。此外,我们分析了热应激条件下卵巢颗粒细胞中铁死亡的机制,结合现有文献总结了热应激与铁死亡之间的潜在关联,并探讨了热应激作用机制中的关键因素,如Nrf2/Keap1、热休克蛋白(HSPs)和c-Jun氨基末端激酶(JNK)的信号通路,并分析了它们在铁死亡过程中可能发挥的作用。最后,本文对未来的研究方向进行了展望,描述了热应激与铁死亡之间可能的相互作用,以期为进一步理解和揭示热应激条件下卵巢颗粒细胞中铁死亡发生的复杂机制提供理论依据。