TREM2 and Sepsis: Zhuang et al. [46] showed that H2 treatment downregulated the expression of phosphomammalian target of rapamycin (p-mTOR)/mTOR and p62 in LPS-treated neuroglial cells and increased the expression of phospho-AMP-activated protein kinase (p-AMPK)/AMPK, light chain 3 (LC3) II/LC3 I, triggering receptor expressed on myeloid cells 2 (TREM-2), and Beclin-1 to activate autophagy and attenuate neuroinflammation in sepsis.