Review Article Discusses Metabolic Reprogramming of Tumor-Associated Macrophages (TAMs)

Cancer is a complex disease and although billions of dollars have been spent on finding safe and effective therapeutics for it, there is still scope for significant development. Researchers have targeted a variety of biological entities and processes to treat cancer. One example is the metabolic processes that reprogram tumor-associated macrophages (TAMs), immune cells that play a crucial role in the development and progression of cancer. Under normal circumstances, macrophages--white blood cells that engulf and kill microorganisms, eliminate dead cells, and stimulate the immune system--safeguard the body against disease. However, TAMs do something significantly odd: they participate in the formation of the tumor microenvironment (TME), thus harming the body. Depending on the environmental stimulus and metabolic processes, macrophages differentiate into two classes: anti-tumor M1-like and pro-tumor M2-like macrophages. The latter resemble TAMs. Whereas M1-like macrophages inhibit tumor growth, M2-like macrophages do the exact opposite and thus play a key role in the proliferation of cancer cell. Researchers from China recently conducted a literature survey—which was published in Volume 135, Issue 20, of the Chinese Medical Journal on 20 October 2022to better understand how this happens. Says Prof. Yi Zhang, corresponding author of the article, and Professor and Director of the Biotherapy Center and Cancer Center at The First Affiliated Hospital of Zhengzhou University, “Peripheral blood-polarized and tissue-resident TAMs constitute a tremendous segment of infiltrating myeloid cells in the TME of most malignant solid tumors. Importantly, TAMs display proangiogenic properties. In this review, we elucidate the metabolic reprogramming of TAMs and explore how they sustain immunosuppression to provide a perspective for potential metabolic therapies.” The open-access review article is titledMetabolic Reprogramming in the Immunosuppression of Tumor-Associated Macrophages.”

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