Csf1, also known as macrophage colony-stimulating factor 1, is the primary growth factor essential for the control of monocyte and macrophage differentiation, survival, proliferation and renewal [3]. It plays a crucial role in the CSF1/CSF1R signaling pathway, which is involved in many biological processes such as bone remodeling, hematopoiesis, and tumor microenvironment regulation [2,1].

In a mouse model, depletion of Csf1 in marrow adipogenic precursors (MALPs) using AdipoqCre (Csf1 CKOAdipoq mice) led to increased femoral trabecular bone mass, diminished osteoclasts in the femoral secondary spongiosa region, and reduced bone marrow cellularity, hematopoietic progenitors, and macrophages, demonstrating that MALPs-synthesized Csf1 controls bone remodeling and hematopoiesis [2]. In the context of tumors, inhibitors of the CSF1/CSF1R signaling pathway, like pexidartinib (PLX3397), can reprogram tumor-associated macrophages (TAMs), stimulate T-cell infiltration, and suppress primary tumor growth and lung metastasis in an osteosarcoma orthotopic xenograft model [1].

In conclusion, Csf1 is vital for the development, homeostasis, and tissue repair related to monocyte and macrophage functions. Gene-knockout (KO) and conditional-knockout (CKO) mouse models have been instrumental in revealing its role in bone-related diseases and cancer. Understanding Csf1's functions through these models provides potential therapeutic targets for treating diseases associated with abnormal macrophage regulation and bone metabolism.