线粒体在细胞代谢和生物能量学中发挥着至关重要的作用，协调各种细胞过程，包括能量产生、新陈代谢、压力适应和氧化还原平衡。此外，线粒体通过与多种信号通路的协调来调节细胞代谢稳态。重要的是，p38 丝裂原激活蛋白激酶 (MAPK) 信号通路在与线粒体的复杂通讯中发挥着关键作用，影响各种功能。本综述探讨了线粒体和 p38 MAPK 信号传导之间的多方面相互作用以及对代谢改变的后续影响。总体而言，p38 MAPK 通路控制关键线粒体蛋白的活性，这些蛋白参与线粒体生物发生、氧化磷酸化、产热和铁稳态。此外，p38 MAPK 通过与其他负责能量稳态的途径协调，有助于调节线粒体对癌症治疗或天然物质诱导的氧化应激和细胞凋亡的反应。因此，这些相互关联的途径的失调可能导致以异常代谢为特征的各种病理。因此，更深入地了解线粒体和 p38 MAPK 通路之间的相互作用及其影响，为癌症和其他以代谢失调为特征的疾病的新型治疗干预措施提供了令人兴奋的预测。版权所有 © 2024 Elsevier Inc. 保留所有权利。

Mitochondria play a crucial role in cellular metabolism and bioenergetics, orchestrating various cellular processes, including energy production, metabolism, adaptation to stress, and redox balance. Besides, mitochondria regulate cellular metabolic homeostasis through coordination with multiple signaling pathways. Importantly, the p38 mitogen-activated protein kinase (MAPK) signaling pathway is a key player in the intricate communication with mitochondria, influencing various functions. This review explores the multifaced interaction between the mitochondria and p38 MAPK signaling and the consequent impact on metabolic alterations. Overall, the p38 MAPK pathway governs the activities of key mitochondrial proteins, which are involved in mitochondrial biogenesis, oxidative phosphorylation, thermogenesis, and iron homeostasis. Additionally, p38 MAPK contributes to the regulation of mitochondrial responses to oxidative stress and apoptosis induced by cancer therapies or natural substances by coordinating with other pathways responsible for energy homeostasis. Therefore, dysregulation of these interconnected pathways can lead to various pathologies characterized by aberrant metabolism. Consequently, gaining a deeper understanding of the interaction between mitochondria and the p38 MAPK pathway and their implications presents exciting forecasts for novel therapeutic interventions in cancer and other disorders characterized by metabolic dysregulation.Copyright © 2024 Elsevier Inc. All rights reserved.