Lipid metabolism reprogramming is the key mechanism for tumor cells to meet the material and energy required for rapid proliferation. This process involves the comprehensive remodeling of fatty acids, cholesterol, and phospholipid metabolic networks, and drives malignant transformation and disease progression by synergistically regulating the core links of lipid synthesis, uptake, transport, oxidation, and storage. Among them, the reprogramming of fatty acid metabolism plays a key carcinogenic driving role, and its abnormal regulation runs through the whole process of tumor development. Hematological malignancies are characterized by rapid proliferation and high metabolic demands, and rely on the lipid-rich bone marrow microenvironment. For this reason, tumor cells establish unique metabolic adaptability by reconstructing the key metabolic pathways of fatty acids to resist stress such as hypoxia and nutritional deficiency. This metabolic reorganization not only enhances the proliferation and survival advantages but also enhances stemness, promotes chemotherapy resistance, and disrupts signaling pathways, thus constituting a critical basis for disease progression. Targeting the dysregulated fatty acid metabolism has become a highly promising treatment direction, providing new possibilities for the precise risk stratification and improvement of therapeutic effect in different subtypes of hematological malignancies. This review systematically summarizes and critiques the recent important findings in this field. By integrating the framework of metabolic vulnerability and disease heterogeneity, it deeply analyzes its molecular mechanism and biological function, and comments on current and emerging metabolic targeted interventions, aiming to provide a new perspective for the development of precision medicine based on metabolic dependence.
Li et al. (Sun,) studied this question.
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