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应激适应的神经内分泌和细胞机制:从中枢神经系统的激素影响到线粒体功能障碍和氧化应激。

Neuroendocrine and cellular mechanisms in stress resilience: From hormonal influence in the CNS to mitochondrial dysfunction and oxidative stress.

机构信息

Department of Pharmacology, Calcutta Institute of Pharmaceutical Technology and AHS, Uluberia, West Bengal, India.

Department of Pharmaceutical Biotechnology, Calcutta institute of pharmaceutical technology and AHS, Uluberia, West Bengal, India.

出版信息

J Cell Mol Med. 2024 Apr;28(7):e18220. doi: 10.1111/jcmm.18220.

Abstract

Recent advancements in neuroendocrinology challenge the long-held belief that hormonal effects are confined to perivascular tissues and do not extend to the central nervous system (CNS). This paradigm shift, propelled by groundbreaking research, reveals that synthetic hormones, notably in anti-inflammatory medications, significantly influence steroid psychosis, behavioural, and cognitive impairments, as well as neuropeptide functions. A seminal development in this field occurred in 1968 with McEven's proposal that rodent brains are responsive to glucocorticoids, fundamentally altering the understanding of how anxiety impacts CNS functionality and leading to the identification of glucocorticosteroids and mineralocorticoids as distinct corticotropic receptors. This paper focuses on the intricate roles of the neuroendocrine, immunological, and CNS in fostering stress resilience, underscored by recent animal model studies. These studies highlight active, compensatory, and passive strategies for resilience, supporting the concept that anxiety and depression are systemic disorders involving dysregulation across both peripheral and central systems. Resilience is conceptualized as a multifaceted process that enhances psychological adaptability to stress through adaptive mechanisms within the immunological system, brain, hypothalamo-pituitary-adrenal axis, and ANS Axis. Furthermore, the paper explores oxidative stress, particularly its origin from the production of reactive oxygen species (ROS) in mitochondria. The mitochondria's role extends beyond ATP production, encompassing lipid, heme, purine, and steroidogenesis synthesis. ROS-induced damage to biomolecules can lead to significant mitochondrial dysfunction and cell apoptosis, emphasizing the critical nature of mitochondrial health in overall cellular function and stress resilience. This comprehensive synthesis of neuroendocrinological and cellular biological research offers new insights into the systemic complexity of stress-related disorders and the imperative for multidisciplinary approaches in their study and treatment.

摘要

神经内分泌学的最新进展挑战了长期以来的观点,即激素的作用仅限于血管周围组织,而不会延伸到中枢神经系统 (CNS)。这一范式转变是由开创性的研究推动的,揭示了合成激素,特别是在抗炎药物中,对类固醇精神病、行为和认知障碍以及神经肽功能有重大影响。该领域的一个重要发展发生在 1968 年,当时 McEven 提出啮齿动物大脑对糖皮质激素有反应,这从根本上改变了人们对焦虑如何影响 CNS 功能的理解,并导致确定糖皮质激素和盐皮质激素为不同的促皮质激素受体。本文重点关注神经内分泌、免疫和 CNS 在促进压力适应能力方面的复杂作用,这是最近的动物模型研究强调的。这些研究强调了适应能力的积极、补偿和被动策略,支持焦虑和抑郁是涉及外周和中枢系统失调的全身性疾病的概念。适应能力被概念化为一个多方面的过程,通过免疫系统、大脑、下丘脑-垂体-肾上腺轴和自主神经系统轴内的适应性机制增强对压力的心理适应能力。此外,本文探讨了氧化应激,特别是其起源于线粒体中活性氧 (ROS)的产生。线粒体的作用不仅限于 ATP 的产生,还包括脂质、血红素、嘌呤和类固醇合成。ROS 诱导的生物分子损伤会导致显著的线粒体功能障碍和细胞凋亡,强调了线粒体健康在整体细胞功能和压力适应能力中的关键性质。这一神经内分泌学和细胞生物学研究的综合综合为应激相关疾病的系统性复杂性以及在其研究和治疗中采用多学科方法的必要性提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5238/10955164/9465a3577875/JCMM-28-e18220-g010.jpg

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