According to a study published in Cell Death & Disease, scientists at Nagoya University in Japan have discovered two enzymes that play a role in macrophage polarization, a key factor affecting fibrosis. The findings of the study suggest a promising treatment possibility for human patients.
Kidney fibrosis is a deadly inflammatory disease that results in the stiffening and loss of normal function of the kidneys. The disease is associated with a mechanism known as macrophage polarization. Macrophages, which are white blood cells that assist the body in fighting infections and repairing tissues, undergo polarization in response to changes in their microenvironment. This polarization results in two different types of macrophages: M1, which causes inflammation, and M2, which possesses anti-inflammatory and tissue repair capabilities.
Because macrophage polarization is tightly controlled and involves multiple signaling pathways and regulatory networks, imbalances in this process are common in many inflammatory diseases. In patients with kidney fibrosis, there is an imbalance between M1 and M2 macrophages. In this situation, M2 macrophages, which normally suppress inflammation, proliferate excessively and secrete factors that promote fibrosis.
Although these imbalances may be therapeutic targets, this is hampered by the fact that the mechanism of macrophage polarization involved in kidney fibrosis is still poorly understood. Furthermore, the molecular mechanisms of macrophage polarization have little in common between mice and humans, making it difficult to translate research results obtained in mice to human diseases.
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As its name suggests, TG2 is involved in the cross-linking of amino DOI: 10.1038/s41419-023-05622-5