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After an injury, macrophages are the focus of liver healing

The liver is famous for its remarkable ability to regenerate, but this healing power depends heavily on the effects of its resident immune cells. A new study shows macrophages that the liver cleaning and repair specialists, and shows that these cells quickly adapt after injuries to clarify debris and support tissue restoration.

Researchers at the National Institutes of Health used advanced imaging and genetic sequencing techniques to examine how different types of macrophages behave in healthy and injured mouse liver. Their results offer new insights into the immune landscape of the liver and indicate new opportunities to improve recovery after damage.

We not only wanted to understand how many macrophages were present, but what they did and where they were“Said Feng.

The team used a combination of multiplex immune fluorescent coloring and single cell RNA sequencing, technologies that enable great detailed mapping of cells and their gene expression patterns. In healthy liver, resident Kupffer cells dominated and made up more than 80 percent of the immune cell population. These cells were not evenly distributed, grouped close to certain blood vessels and showed high phagocytosis levels, the process of interlacing pathogens and dead cells.

This balance changed dramatically. Using models of an acute liver injury, including exposure to Concanavalin A and Paracetamol, the researchers observed an increase in the macrophages derived from monocytes that infiltrated the liver. These newcomer cells differed in both place and in the function of Kupapfer cells. They grouped around necrotic lesions and expressed genes that were involved in the deposition and redesign of the tissue.

We have identified several populations of macrophages that seem to specialize in different stages of the reaction of the injuries.“Said Feng.

Some macrophages derived from monocytes were rich in proteins that dismantle cellular rubble, while other markers expressed the tissue repair. A sub -group even showed a high endotheline conversion enzyme 1, which indicates a role in the control of the blood vessel behavior and the fibrosis during healing.

The study may have been most fascinating how macrophages multiply and die during the injury. In healthy liver, the macrophage turnover was low. After an injury, both the proliferation and apoptosis rates dramatically increased, which indicates that the liver quickly converted their immune workforce in response to damage.

Seeing the expansion and wear and tear of macrophages in real time offers a more comprehensive picture of how dynamic these cells are during the liver injury and repair.“Said Feng.

The results have promising effects on future therapies. Targeting specific macrophage populations could help accelerate liver healing or prevent fibrosis, a scarring process that can lead to chronic liver diseases. By improving the functions of useful macrophages or the limitation of harmful restrictions, clinicians may devote their balance to recovery.

Our next step is to test whether the increase in certain macrophage populations can improve the cure results in chronic models with liver diseases.“Said Feng.

In addition to their therapeutic potential, the methods of the study offer a blueprint for examining immune responses in other organs. The combination of spatial mapping with genetic profil creation could show how different cell types interact while disease processes interact in the body elsewhere.

While more work is necessary to translate these results into treatments, the study represents a leap forward when understanding the immunchoreography of the liver. By observing the disassembly teams of the liver in action, they discover new strategies to support the legendary resistance of the organ.

Source:

First hospital at Jilin University

Journal Reference:

Feng, d. ,, et al. (2025). Characterization of macrophages in healthy and sick liver in mice: identification of necrotic lesion -associated macrophages. Egastroenterology. doi.org/10.1136/egastro 2025-100189.

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