代谢平衡和疾病中的 mTOR。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY Experimental cell research Pub Date : 2024-07-22 DOI:10.1016/j.yexcr.2024.114173
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引用次数: 0

摘要

维持细胞代谢平衡的能力对生命至关重要,而 mTOR 在其中发挥着重要作用。这种激酶整合上游营养信号,通过增加新陈代谢和抑制自噬,在生理和新陈代谢中发挥重要功能。因此,mTOR 活性失调会导致疾病,尤其是代谢性疾病,如癌症、2 型糖尿病和神经系统疾病。因此,抑制过度激活的 mTOR 成为治疗各种代谢性疾病的合理方法。在这篇综述中,我们将讨论 mTOR 如何对上游信号做出反应,以及 mTOR 如何调节包括蛋白质、核酸和脂质代谢在内的代谢过程。此外,我们还讨论了 mTOR 信号活动失调的可能原因和后果,并总结了相关应用,如抑制 mTOR 活性以治疗这些疾病。这篇综述将推动我们全面了解 mTOR 与代谢平衡之间的关系,这对人类健康具有重大影响。
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mTOR in metabolic homeostasis and disease

The ability to maintain cellular metabolic homeostasis is critical to life, in which mTOR plays an important role. This kinase integrates upstream nutrient signals and performs essential functions in physiology and metabolism by increasing metabolism and suppressing autophagy. Thus, dysregulation of mTOR activity leads to diseases, especially metabolic diseases such as cancer, type 2 diabetes and neurological disorders. Therefore, inhibition of overactivated mTOR becomes a rational approach to treat a variety of metabolic diseases. In this review, we discuss how mTOR responds to upstream signals and how mTOR regulates metabolic processes, including protein, nucleic acid, and lipid metabolism. Furthermore, we discuss the possible causes and consequences of dysregulated mTOR signaling activity, and summarize relevant applications, such as inhibition of mTOR activity to treat these diseases. This review will advance our comprehensive knowledge of the association between mTOR and metabolic homeostasis, which has significant ramifications for human health.

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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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