The study showed that specifically removing KLK7 from macrophages significantly reduced inflammation and improved insulin sensitivity in obese mice. In the absence of KLK7, immune cells were less likely to infiltrate adipose tissue and adopt a pro-inflammatory state. Further analysis indicated that KLK7 plays a critical role in regulating the energetic state and mobility of immune cells, influencing their ability to promote inflammation.
The researchers also found that higher levels of KLK7 were associated with increased inflammation in human adipose tissue and blood samples, supporting its role in obesity-related metabolic dysfunction. These findings suggest that targeting KLK7 could provide a promising new approach to treating obesity-related metabolic disorders and highlight the potential for the development of KLK7-specific inhibitors. Unlike conventional weight loss therapies, inhibition of KLK7 may help control inflammation and insulin resistance independently of weight loss. This study was supported by the CRC 1052 “Obesity Mechanisms”.
Original Publication
Ribas-Latre et.al., 2025: The serine protease KLK7 promotes immune cell infiltration in visceral adipose tissue in obesity. Metabolism. DOI: 10.1016/j.metabol.2025.156239
