Inhibiting metastasis is the key to the treatment of malignant tumors. During the development of tumors, the microenvironment plays a significant role, and hypoxia is one of its important characteristics. Exosomes, as an important component of the microenvironment, connect tumor cells with the hypoxic microenvironment and mediate information exchange between cells. Tumor cells secrete more exosomes than normal cells, and hypoxia further stimulates their release. Hypoxia-induced tumor-derived exosomes carry stable genetic material and play key regulatory roles in promoting tumor proliferation, establishing a pre-metastasis microenvironment, and accelerating angiogenesis. This article comprehensively reviews the mechanisms by which tumor-derived exosomes regulate tumor proliferation and metastasis in a hypoxic microenvironment, which has potential clinical significance.
Objective To systematically summarize the role of immune cells in the progression of anastomotic leak (AL) following colorectal cancer (CRC) surgery, with an emphasis on the molecular mechanisms of metabolic reprogramming in relevant immune cells, aiming to provide new insights for the diagnosis and treatment of AL. MethodWe reviewed recent literature on the metabolic reprogramming of immune cells in AL following CRC surgery. ResultsIn the postoperative CRC AL microenvironment, homeostasis imbalance drives metabolic reprogramming of immune cells (macrophages, neutrophils), manifested as enhanced glycolysis, impaired fatty acid oxidation, and tricarboxylic acid cycle disruption. Accumulated metabolites (lactate, succinate), along with acidic pH, hypoxia, and immune factors, collectively shape an intertwined immunosuppressive and pro-inflammatory microenvironment that impedes anastomotic healing. Targeting key nodes in this metabolic reprogramming offers potential therapeutic strategies and a theoretical framework for clinical translation in AL. ConclusionsImmune cells, as key components of the AL microenvironment, play an important role in the initiation and progression of AL. In-depth exploration of the molecular mechanisms underlying metabolic reprogramming of relevant immune cells may provide directions for the diagnosis and treatment of AL, with the aim of improving patients’ outcomes.