Acute Myeloid Leukemia (AML) is characterized by aggressive proliferation and metabolic reprogramming that support its survival and resistance to therapy. This review explores the metabolic distinctions between AML cells and normal hematopoietic stem cells (HSCs), emphasizing the role of altered mitochondrial function, oxidative phosphorylation (OXPHOS), and biosynthetic pathways in leukemic progression. AML cells exhibit distinct metabolic vulnerabilities, including increased mitochondrial biogenesis, reliance on glycolysis and amino acid metabolism, and unique signaling interactions that sustain leukemic stem cells (LSCs). These dependencies provide potential therapeutic targets, as metabolic inhibitors have demonstrated efficacy in disrupting AML cell survival while sparing normal hematopoietic cells. We examine current and emerging metabolic therapies, such as inhibitors targeting glycolysis, amino acid metabolism, and lipid biosynthesis, highlighting their potential in overcoming drug resistance. However, challenges remain in translating these strategies into clinical practice due to AML’s heterogeneity and adaptability. Further research into AML’s metabolic plasticity and precision medicine approaches is crucial for improving treatment outcomes. Understanding and exploiting AML’s metabolic vulnerabilities could pave the way for novel, more effective therapeutic strategies.
急性髓系白血病（AML）以恶性增殖和代谢重编程为特征，这些过程支持其存活及治疗抵抗。本综述探讨AML细胞与正常造血干细胞（HSC）之间的代谢差异，重点阐述线粒体功能改变、氧化磷酸化（OXPHOS）及生物合成通路在白血病进展中的作用。AML细胞表现出独特的代谢脆弱性，包括线粒体生物合成增强、对糖酵解和氨基酸代谢的依赖，以及维持白血病干细胞（LSC）的特异性信号交互。这些代谢依赖性为治疗提供了潜在靶点，代谢抑制剂已显示出在破坏AML细胞存活的同时保护正常造血细胞的疗效。本文系统评述当前及新兴的代谢疗法，如针对糖酵解、氨基酸代谢和脂质生物合成的抑制剂，并强调其在克服耐药性方面的潜力。然而，由于AML的异质性和适应性，将这些策略转化为临床实践仍面临挑战。进一步研究AML的代谢可塑性及精准医疗方法对改善治疗结局至关重要。深入理解并利用AML的代谢脆弱性，可能为开发新型、更有效的治疗策略开辟道路。
肿瘤(癌症)患者之家