Tgm2 alleviates LPS-induced apoptosis by inhibiting JNK/BCL-2 signaling pathway through interacting with Aga in macrophages

Sepsis is an unusual systemic infection caused by bacteria, which is a life-threatening organ dysfunction. The innate immune system plays an important role in this process; however, the specific mechanisms remain unclear. Using the LPS + treated mouse model, we found that the survival rate of Tgm2-/- mice was lower than that of the control group, while the inflammation was much higher. We further showed that Tgm2 suppressed apoptosis by inhibiting the JNK/BCL-2 signaling pathway. More importantly, Tgm2 interacted with Aga and regulated mitochondria-mediated apoptosis induced by LPS. Our findings elucidated a protective mechanism of Tgm2 during LPS stimulation and may provide a new reference target for the development of novel anti-infective drugs from the perspective of host immunity.

Automated summary

The study revealed a protective role of Tgm2 in sepsis, showing that it can suppress apoptosis by inhibiting the JNK/BCL-2 signaling pathway and regulating mitochondria-mediated apoptosis. This highlights Tgm2 as a potential target for the development of novel anti-infective drugs.