Microglia and macrophages play critical roles in glioma progression and maintenance. These cells, which are part of the tumor microenvironment, contribute to tumor growth, survival, and invasion by releasing growth factors, cytokines, and chemokines. They also support the tumor's ability to resist treatment. In gliomas, microglia and macrophages can be of intrinsic or peripheral origin, and their interactions with cancer cells create a supportive stroma that promotes tumor development. Recent studies suggest that targeting these cells could be a promising therapeutic strategy for gliomas, which are difficult to treat with conventional methods. Microglia, the resident macrophages of the central nervous system, originate from yolk sac progenitors and are distinct from blood-derived monocytes. However, the distinction between microglia and macrophages is not always clear, as both can be involved in glioma progression. The role of microglia in glioma biology is further supported by studies showing that they contribute to tumor growth and invasion. For example, in low-grade gliomas, microglia and macrophages are present in significant numbers and are associated with tumor progression. In high-grade gliomas, microglia can be polarized into different phenotypes, such as M1 or M2, which have distinct functions in tumor progression. TAMs (tumor-associated macrophages) are recruited to the glioma environment and can be influenced by various factors, including chemokines and growth factors. They contribute to tumor growth by promoting angiogenesis, invasion, and the survival of glioma cells. TAMs also interact with glioma stem cells, which are critical for tumor recurrence and resistance to treatment. The activation and polarization of TAMs can be influenced by various signaling pathways, including those involving CSF-1, TGF-β, and MMPs. Targeting TAMs is an emerging area of glioma research, with potential therapeutic strategies including the inhibition of CSF-1 signaling, modulation of TAM polarization, and the use of drugs that alter TAM function. These approaches aim to disrupt the supportive role of TAMs in glioma progression and improve treatment outcomes. Overall, the complex interactions between TAMs and glioma cells highlight the importance of understanding the tumor microenvironment in developing effective therapies for gliomas.Microglia and macrophages play critical roles in glioma progression and maintenance. These cells, which are part of the tumor microenvironment, contribute to tumor growth, survival, and invasion by releasing growth factors, cytokines, and chemokines. They also support the tumor's ability to resist treatment. In gliomas, microglia and macrophages can be of intrinsic or peripheral origin, and their interactions with cancer cells create a supportive stroma that promotes tumor development. Recent studies suggest that targeting these cells could be a promising therapeutic strategy for gliomas, which are difficult to treat with conventional methods. Microglia, the resident macrophages of the central nervous system, originate from yolk sac progenitors and are distinct from blood-derived monocytes. However, the distinction between microglia and macrophages is not always clear, as both can be involved in glioma progression. The role of microglia in glioma biology is further supported by studies showing that they contribute to tumor growth and invasion. For example, in low-grade gliomas, microglia and macrophages are present in significant numbers and are associated with tumor progression. In high-grade gliomas, microglia can be polarized into different phenotypes, such as M1 or M2, which have distinct functions in tumor progression. TAMs (tumor-associated macrophages) are recruited to the glioma environment and can be influenced by various factors, including chemokines and growth factors. They contribute to tumor growth by promoting angiogenesis, invasion, and the survival of glioma cells. TAMs also interact with glioma stem cells, which are critical for tumor recurrence and resistance to treatment. The activation and polarization of TAMs can be influenced by various signaling pathways, including those involving CSF-1, TGF-β, and MMPs. Targeting TAMs is an emerging area of glioma research, with potential therapeutic strategies including the inhibition of CSF-1 signaling, modulation of TAM polarization, and the use of drugs that alter TAM function. These approaches aim to disrupt the supportive role of TAMs in glioma progression and improve treatment outcomes. Overall, the complex interactions between TAMs and glioma cells highlight the importance of understanding the tumor microenvironment in developing effective therapies for gliomas.