The Akt/mTOR signaling pathway governs macromolecules synthesis, cell growth and metabolism in response to nutrients and growth factors. REDD1 is a conserved and ubiquitous protein, which is transiently induced in response to multiple stimuli. Acting like an endogenous inhibitor of the Akt/mTOR signaling pathway, REDD1 protein has been shown to regulate cell growth, mitochondrial function, oxidative stress and apoptosis. Recent studies also indicate that timely REDD1 expression limits Akt/mTOR-dependent synthesis processes to spare energy during metabolic stresses, avoiding energy collapse and detrimental consequences. In contrast to this beneficial role for metabolic adaptation, REDD1 chronic expression appears involved in the pathogenesis of several diseases. Indeed, REDD1 expression is found as an early biomarker in many pathologies including inflammatory diseases, cancer, neurodegenerative disorders, depression, diabetes and obesity. Moreover, prolonged REDD1 expression is associated with cell apoptosis, excessive ROS production and inflammation activation leading to tissue damages. In this review, we decipher several mechanisms that make REDD1 a likely metabolic double agent depending on its duration of expression in different physiological and pathological contexts. We also discuss the role played by REDD1 in the crosstalk between the Akt/mTOR signaling pathway and the energetic metabolism.

中文翻译：

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REDD1是代谢双重药物吗？生理学和病理学的教训。

Akt / mTOR信号传导途径控制大分子的合成，细胞生长和代谢，以响应营养物质和生长因子。REDD1是一种保守且普遍存在的蛋白质，可响应多种刺激而短暂诱导。REDD1蛋白像Akt / mTOR信号传导途径的内源抑制剂一样发挥作用，可调节细胞生长，线粒体功能，氧化应激和细胞凋亡。最近的研究还表明，及时的REDD1表达限制了Akt / mTOR依赖的合成过程以在代谢压力期间节省能量，避免了能量崩溃和有害后果。与这种对代谢适应的有益作用相反，REDD1慢性表达似乎与几种疾病的发病机制有关。确实，发现REDD1表达是许多病理学中的早期生物标志物，包括炎性疾病，癌症，神经退行性疾病，抑郁症，糖尿病和肥胖症。而且，REDD1的延长表达与细胞凋亡，ROS产生过多和炎症激活导致组织损伤有关。在这篇综述中，我们根据其在不同生理和病理环境中的表达持续时间，来解读几种使REDD1成为可能的代谢双重药物的机制。我们还讨论了REDD1在Akt / mTOR信号传导途径与能量代谢之间的串扰中发挥的作用。过量的ROS产生和炎症活化导致组织损伤。在这篇综述中，我们根据其在不同生理和病理环境中的表达持续时间，来解读几种使REDD1成为可能的代谢双重药物的机制。我们还讨论了REDD1在Akt / mTOR信号传导途径与能量代谢之间的串扰中发挥的作用。过量的ROS产生和炎症活化导致组织损伤。在这篇综述中，我们根据其在不同生理和病理环境中的表达持续时间，来解读几种使REDD1成为可能的代谢双重药物的机制。我们还讨论了REDD1在Akt / mTOR信号传导途径与能量代谢之间的串扰中发挥的作用。