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. Ki
Enzyme-regulating macrophages found in both humans and mice open the door to translating findings in mice into human therapies. Credit: Issey Takahashiin 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.
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.
“Macrophage polarization, which promotes fibrosis through cross-linking enzymes, has a similar induction mechanism in both humans and mice,” Tatsukawa said. “By targeting the regulation of macrophage function, we hope to develop treatments for various diseases caused by an imbalance between the promotion and suppression of inflammation, such as fibrosis, cancer, and atherosclerosis.”
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