Kang Lab

The Kang Laboratory is dedicated to elucidating mechanisms underlying chronic inflammatory lung diseases and critical illness, with a central focus on dysregulated mitochondrial innate immune signaling. Over the past decade, our research has positioned mitochondria as pivotal hubs of innate immune regulation whose dysfunction drives age-related pulmonary diseases, including COPD, idiopathic pulmonary fibrosis (IPF), and bacterial sepsis.

A defining theme is the mitochondrial antiviral signaling protein (MAVS) and its roles beyond canonical antiviral defense. We have demonstrated that MAVS is indispensable for pulmonary fibrosis and that PINK1 modulates MAVS multimeric aggregation, linking mitochondrial quality control to innate immune dysregulation. Our most recent work extends this paradigm to bacterial sepsis, where MAVS aggregation amplifies hyperinflammation through pyroptotic cell death and DAMP release, forming a feed-forward loop of systemic injury.

Complementing these findings, NLRX1 deficiency induces NAD⁺ decline, mTOR activation, and cellular senescence, accelerating aging lung-like phenotypes, while VISTA (PD-1H) functions as a critical immune checkpoint that limits pulmonary fibrosis. Together, these discoveries illuminate how aging biology converges with mitochondrial immune dysfunction to drive chronic lung diseases.

Our research integrates cell-specific conditional knockout and transgenic mouse models, transcriptomic analyses, and functional assays of immune signaling and cell death. Publications from our laboratory have been consistently highlighted through editorial commentaries in the Journal of Clinical Investigation, American Journal of Respiratory and Critical Care Medicine, and European Respiratory Journal, and we remain committed to translating these discoveries into therapeutic strategies that improve outcomes for patients with lung disease and critical illness.

1. Mitochondrial dysfunction and mitophagy in COPD
2. NLRX1-inhibiting-MAVS-dependent inflammasome in COPD and Cs- and virus-associated disorders
3. Role(s) of Interleukin-18 in pulmonary inflammation and tissue remodeling responses