The prevalence of chronic kidney disease (CKD) is increasing worldwide, making the disease an urgent clinical challenge. Caloric restriction has various anti-aging and organ-protective effects, and unraveling its molecular mechanisms may provide insight into the pathophysiology of CKD. In response to changes in nutritional status, intracellular nutrient signaling pathways show adaptive changes. When nutrients are abundant, signals such as mechanistic target of rapamycin complex 1 (mTORC1) are activated, driving cell proliferation and other processes. Conversely, others, such as sirtuins and AMP-activated protein kinase, are activated during energy scarcity, in an attempt to compensate. Autophagy, a cellular self-maintenance mechanism that is regulated by such signals, has also been reported to contribute to the progression of various kidney diseases. Furthermore, in recent years, ketone bodies, which have long been considered to be detrimental, have been reported to play a role as starvation signals, and thereby to have renoprotective effects, via the inhibition of mTORC1. Therefore, in this review, we discuss the role of mTORC1, which is one of the most extensively studied nutrient-related signals associated with kidney diseases, autophagy, and ketone body metabolism; and kidney energy metabolism as a novel therapeutic target for CKD.

慢性肾脏病（CKD）的患病率在全球范围内不断增加，使该疾病成为紧迫的临床挑战。热量限制具有多种抗衰老和器官保护作用，揭示其分子机制可能有助于深入了解 CKD 的病理生理学。为了响应营养状况的变化，细胞内营养信号通路表现出适应性变化。当营养丰富时，雷帕霉素复合物 1 (mTORC1) 机械靶标等信号被激活，驱动细胞增殖和其他过程。相反，其他蛋白，如去乙酰化酶和 AMP 激活蛋白激酶，在能量短缺时被激活，以试图进行补偿。自噬是一种受此类信号调节的细胞自我维护机制，据报道也有助于各种肾脏疾病的进展。此外，近年来，长期以来被认为有害的酮体据报道发挥饥饿信号的作用，从而通过抑制mTORC1 发挥肾脏保护作用。因此，在这篇综述中，我们讨论了 mTORC1 的作用，mTORC1 是研究最广泛的与肾脏疾病、自噬和酮体代谢相关的营养相关信号之一；和肾脏能量代谢作为 CKD 的新治疗靶点。