慢性炎症,脂肪晶体 z-bo 2020-10-08 326

　　According to a new study published in the journal Autophagy, researchers at the University of Bonn found that congenital fat metabolism disorders can lead to chronic inflammation of the immune system. In recent years, it has been discovered that some potential mutations can change the activity of key enzymes in fat metabolism, so that human cells produce about ten times more deoxysphingolipids than normal cells. I will. At high concentrations, it will form crystal-like clumps in the affected cells.

　　Fat crystals have great damage to mitochondrial function, and cell types with high energy requirements will suffer more damage. Specifically, this symptom mainly affects nerve cells, which is why you experience pain and other neurological symptoms. In their current study, the researchers also found mitochondrial defects in connective tissue cells in mice.

　　Researchers examined mouse macrophages. The results indicate that macrophages, such as nerve or connective tissue cells, produce large amounts of deoxysphingolipids during the course of the disease. At the same time, they absorb abnormal fat from dead cells. In other words, the number of fat crystals they get is several times that of other cell types. This process significantly disrupts the functions of various cellular components (such as mitochondria) of these macrophages. In addition, this process also activates the autophagy response of macrophages, and at the same time activates the molecular complex called the lower body that promotes inflammation. The activated stromal bodies cause macrophages to release inflammatory messenger molecules. In this way, other immune cells further enhance this effect.

　　This result may bring new inspiration to common diseases. For unknown reasons, the production of deoxysphingolipids in certain cells of diabetic patients is also significantly increased. In diabetes, doctors often observe severe chronic inflammation, exacerbating the serious consequences of the disease. This study provides an explanation for this new molecular mechanism of clinical manifestations.