專業
Helicobacter pylori infection and pathogenesis
Helicobacter pylori infection affects more than 50% of the world’s population and is associated with a wide spectrum of clinical outcomes, including gastritis, peptic ulcer, and gastric cancer. Lipopolysaccharide (LPS), a major surface antigen of Gram-negative bacteria, is essential for the physical integrity and function of the bacterial outer membrane. Beyond maintaining outer membrane integrity and enabling host evasion, LPS biosynthesis shares enzymes with those that glycosylate H. pylori adhesins and virulence factors, supports the formation of outer membrane vesicles (OMVs), and modulates the immune response. By integrating bacterial glycobiology, outer membrane vesicle biology, and host innate immunology, our research aims to establish a novel pathogenic framework linking LPS biosynthesis, protein glycosylation, and non-canonical virulence mechanisms to H. pylori infection, providing an important foundation for future basic and translational research in infectious diseases.
Functions, pathophysiology and therapeutic intervention of human mitochondrial complex I
Among the five enzyme complexes in the oxidative phosphorylation system (OXPHOS), human complex I is the most intricate membrane-bound enzyme known to date. Dysfunction in this enzyme complex has been linked to a wide variety of mitochondrial and neurodegenerative diseases (including Parkinson’s disease), and is also involved in the aging process. The underlying genetic defect may lie in either mtDNA or nuclear DNA. Because of the enzyme's complexity and its dual genetic origins, most complex I defects still lack an identified pathogenic mechanism, and no effective remedies have been established for complex I deficiencies. We aim to understand the proton-pumping and electron-transferring mechanisms of human complex I, reveal the functional and structural roles of its component subunits, and develop novel approaches to treat mitochondrial diseases caused by complex I deficiencies.