There is a bidirectional association between tumor-associated macrophage (TAM) and colorectal cancer. Small molecular substances metabolized by colorectal cancer affect the reprogramming of TAM, and TAM in turn regulates the biological behavior of colorectal cancer cells by secreting small molecular substances, and promotes the progression of colorectal cancer. In addition, gut microbiota metabolites are closely related to TAM reprogramming, and intestinal flora imbalance leads to gut barrier damage, favoring bacterial translocation and causing chronic tumorigenic inflammation. Studying the reprogramming mechanism affecting TAM and its relationship with the occurrence and development of colorectal cancer may provide new ideas for the study of immunotherapy in patients with colorectal cancer. This article reviews the research progress of TAM in patients with colorectal cancer, aims to provide a reference for clinical research.
The poor treatment effect and short survival period of patients with acute leukemia are mainly due to the lack of effective early diagnosis and treatment targets. Lipid metabolism reprogramming meets the material and energy requirements for rapid proliferation and division of tumor cells, and is associated with the invasiveness, recurrence, and chemotherapy resistance of acute leukemia. This article reviews the carcinogenic and chemotherapy resistance mechanisms of lipid metabolism reprogramming in leukemia cells, and summarizes the latest findings on targeted fatty acid metabolism pathways, aiming to provide a new perspective on the role of intracellular fatty acid metabolism in the occurrence and development of acute leukemia. It is expected to provide a theoretical basis for the elucidation of its resistance mechanism and the development of corresponding targeted therapies.
Age-related macular degeneration (AMD) involves dysregulation of the innate immune response of complement and mononuclear phagocytes and abnormalities of local microglia. When microglia transition from a resting state to an active state, their metabolic pathway also changes, known as "metabolic reprogramming", and their glucose metabolic reprogramming is a key factor in the pathogenesis of AMD, involving multiple signaling pathways. Including phosphatidylinositol 3-kinase-serine threonine kinase-rapamycin target, adenylate activated protein kinase and hypoxia-inducing factor 1 pathway. These metabolic changes regulate the inflammatory response, energy supply, and neuroprotective functions of microglia. Therapeutic strategies to regulate the reprogramming of glucose metabolism in microglia have achieved initial results. Future studies should further explore the mechanisms of microglia metabolic regulation to develop new targeted drugs and intervene in the treatment of AMD through anti-cellular aging pathways.