Tumor microenvironment consists of malignant and non-malignant cells. The interaction of these dynamic and different cells is responsible for tumor progression at different levels. The non-malignant cells in TME contain cells such as tumor-associated Macrophages (TAMs), cancer associated fibroblasts, pericytes, adipocytes, T cells, B cells, myeloid-derived suppressor cells (MDSCs), tumor-associated neutrophils (TANs), dendritic cells (DCs) and Vascular endothelial cells. TAMs are abundant in most human and murine cancers and their presence are associated with poor prognosis. The major event in tumor microenvironment is macrophage polarization into tumor-suppressive M1 or tumor-promoting M2 types. Although much evidence suggests that TAMS are primarily M2-like Macrophages, the mechanism responsible for polarization into M1 and M2 Macrophages remain unclear. TAM contributes cancer cell motility, invasion, metastases and angiogenesis. The relationship between TAM and tumor cells lead to used them as a diagnostic marker, therapeutic target and prognosis of cancer. This review presents the origin, polarization, role of TAMs in inflammation, metastasis, immune evasion and angiogenesis as well as they can be used as therapeutic target in variety of cancer cells. It is obvious that additional substantial and preclinical research is needed to support the effectiveness and applicability of this new and promising strategy for cancer treatment.

Angiogenesis is very important for most strategies for regenerative damaged organs. The natural inflammatory response can be affected by the activity of different types of Macrophages and their cytokines. Macrophages exist in a wide variety of phenotypes. These Macrophages can range from classic M1 to M2 Macrophages. M2 Macrophages themselves can include different types of subgroups. These types of Macrophages are usually effective in vascular regeneration while M1 or classic Macrophages play a role in chronic wounds. The Macrophages move toward the M2 phenotype or inhibit the polarization of the Macrophages toward the M1 phenotype. On the other hand, macrophage polarization can be affected by a variety of factors, such as different types of miRNAs. The process of vascular repair and enhancing the therapeutic potential of drug regulators the treatment of vascular damage through modification of macrophage polarization. Macrophages do this by various mechanisms, which are described in detail in this study. Finally, new therapeutic mechanisms aimed at Macrophages in vascular disease are discussed.

Background: Macrophages play a significant role in both the development and regression of liver fibrosis, engaging in related pro-inflammatory and anti-inflammatory processes. In recent years, an increasing number of studies have elucidated the mechanisms by which Macrophages influence liver fibrosis. Objectives: This bibliometric analysis aims to investigate the research trends in liver fibrosis regulation by Macrophages through a systematic literature review. Methods: We conducted a search for literature, including research articles and reviews, using the keywords 'liver fibrosis and Macrophages' and 'liver cirrhosis and Macrophages' in the Web of Science database, covering the period from 2007 to 2023. We retrieved and analyzed publications on liver fibrosis mediated by Macrophages from the Web of Science Core Collection database on October 8, 2023. Visualization analysis was performed using CreateSpace (version 6.1.R6), VOSviewer (version 1.6.19), and Scimago Graphica (version 1.0.34.0). Results: We identified a total of 1732 records in the WoSCC, of which 1664 papers were ultimately included in our analysis. China emerged as the country with the most significant number of publications, while Germany and the University of California San Diego stood out for their influence, with centralities of 0.41 and 0.14, respectively. Frank Tacke was identified as the most prolific author, contributing 49 papers. Hepatology was the journal with the highest number of publications and citations. The most frequently mentioned keywords in this field were liver fibrosis, expression, hepatic stellate cells, activation, inflammation, and Macrophages. Conclusions: The study of macrophage-mediated liver fibrosis, particularly the mechanisms regulating the heterogeneity of hepatic Macrophages, is a mature and promising research area. Macrophage-based therapies for liver fibrosis are anticipated to be crucial topics in the future. Bibliometric analysis offers valuable insights for future basic research directions and clinical practice.