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.
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.
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.
Müller glial cells (MGCs) are the principal radial glial cells in the retina, extending across all retinal layers and playing a crucial role in maintaining neuronal homeostasis, regulating metabolism, and participating in damage repair. The response patterns of MGCs differ significantly between species: in lower vertebrates, MGCs possess reprogramming and regenerative abilities, while in mammals, they primarily exhibit reactive gliosis. In diabetic retinopathy, MGCs are activated in a hyperglycemic environment, releasing vascular endothelial growth factors and inflammatory cytokines, which disrupt the blood-retinal barrier, leading to macular edema and participating in the maintenance and repair of foveal morphology. In vitreoretinal interface diseases, MGCs serve as the primary source of the internal limiting membrane and provide mechanical support, contributing to the formation and repair of macular holes and epiretinal membranes. In ischemic retinal diseases, MGCs regulate pathological angiogenesis through pathways such as hypoxia-inducible factor-1α, interacting with microglial cells to exacerbate inflammatory damage. In neurodegenerative diseases such as glaucoma, MGCs regulate cholesterol metabolism and release pro-inflammatory cytokines, creating a neurotoxic microenvironment that promotes retinal ganglion cell death. Recent studies investigating signaling pathways, such as Janus kinase/signal transducer and activator of transcription, have revealed the molecular basis underlying the regenerative potential of MGCs. Although the regenerative capacity of MGCs is limited in mammals, strategies such as gene therapy (e.g., overexpression of neurogenic differentiation factor 1), pharmacological interventions (e.g., fibroblast growth factor 21), and cell reprogramming can partially reactivate their regenerative potential and promote retinal neuron regeneration. Future therapeutic strategies should focus on precisely regulating MGC responses to maximize their neuroprotective effects while suppressing glial scar formation, providing new directions for the prevention and treatment of retinal degenerative diseases.
As essential immune cells for retinal homeostasis and repair, macrophages play a pivotal role throughout vascular remodeling, a central pathological feature of diabetic retinopathy (DR). Emerging evidence indicates that macrophages actively adapt to the diabetic microenvironment through metabolic reprogramming. Notably, lipid metabolic reprogramming plays a crucial role in shaping macrophage activation phenotypes, modulating immune functions, and regulating the synthesis of inflammatory mediators, thereby influencing vascular remodeling. A deeper understanding of lipid metabolic reprogramming in macrophage-mediated vascular remodeling may provide novel immunometabolic targets for therapeutic intervention in DR.
