Internal clock affects inflammation, cancer risk and optimal time for treatment
In the body, almost every cell contains an internal clock, a circadian mechanism that synchronizes many processes, including sleep, metabolism, hormone release, and immune system function. When the body encounters an injury or infection, the immune system sends macrophages, cells that trigger an inflammatory response. Macrophages can exist in two states. The pro-inflammatory state (M1) supports inflammation, while the anti-inflammatory state (M2) helps to quell the response and repair tissues. The balance between these conditions is critically important: its violation leads to chronic inflammation, which is associated with the development of cancer, liver disease, diabetes and autoimmune disorders. Scientists from Kyushu University have uncovered a previously unknown mechanism linking circadian rhythms with inflammatory responses of immune cells. The study shows how the circadian clock protein BMAL1 increases inflammation by controlling lipid metabolism in the cell nucleus. The findings may change approaches to the treatment of inflammatory diseases and cancer, including by choosing the optimal time for taking medications.
The researchers found that the protein BMAL1, one of the main components of our internal clock, is responsible for the transition of macrophages to the M1 mode. To test this, they bred special mice. These mice had BMAL1 disabled in their macrophages. Then, they were exposed to a substance that causes liver inflammation and can lead to tumors.
The results were clear. In regular mice, the inflammation increased after exposure to the substance, and more M1 macrophages appeared. In mice without BMAL1, inflammation was significantly weaker, and tumors developed more poorly.
At the cellular level, the mechanism works as follows. BMAL1 finds the enzyme MFP2 in the cell, which is typically responsible for fatty acids in specific compartments of the cell. BMAL1 transports MFP2 to the nucleus, the control center of the cell. There, MFP2 triggers a series of reactions that activate the inflammatory gene switch (known as NF-κB). As a result, macrophages switch to a pro-inflammatory mode.
The most interesting thing is that this process is scheduled. The level of MFP2 in the nucleus changes throughout the day and depends on BMAL1. It increases when BMAL1 is at its highest and decreases when it is at its lowest. This means that the intensity of inflammation can also vary depending on the time of day.
This discovery provides new insights for treatment. For example, it may be possible to block MFP2 in the nucleus or administer medications at a time of day when this mechanism is particularly active, which could lead to better outcomes with fewer side effects.
Now, experts want to test whether this mechanism works in humans. If it does, then in the future, doctors will be able to choose the right time to treat inflammatory diseases and cancer.
Published
June, 2026
Category
Science
Duration of reading
2-3 min
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Source
Scientific journal Cell Reports. Article: The circadian clock component BMAL1 enhances macrophage inflammation by nuclear translocation of peroxisomal β-oxidation enzyme MFP2
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