Our research focuses on understanding the biological functions of the Nogo-B receptor (NgBR) and its roles in human diseases. NgBR is a cell surface receptor I identified during my postdoctoral training at Yale School of Medicine. Our continuous work at the Medical College of Wisconsin has revealed that NgBR is crucial for development, and its absence leads to early embryonic death and vascular abnormalities. In 2019, I joined NYU Grossman Long Island School of Medicine to further investigate how NgBR and its regulators, such as RXR and PPARs, influence metabolic diseases and our body's resilience.
Resilience is our ability to resist, adapt, and recover from physical and environmental challenges. Obesity is a known risk factor for type 2 diabetes (T2D), with over 90% of T2D patients being overweight or obese. However, only about 30% of obese individuals develop T2D, suggesting that certain resilience factors protect against obesity-induced T2D. By comparing gene expression profiles between obese individuals with and without T2D, we found that NgBR might be a resilience factor. Loss of NgBR in the liver due to obesity impairs insulin sensitivity, crucial for preventing T2D. Additionally, our research indicates that high blood sugar levels in diabetes patients may reduce resilience, leading to the vulnerability of severe lung injury. Our recent study demonstrated that NgBR is vital for maintaining blood vessel integrity and mitigating inflammatory lung injury.
Using bioinformatics and animal models, we continue to explore how obesity and diabetes affect resilience and aim to develop interventions to enhance resilience against metabolic diseases. Our research bridges laboratory findings with clinical applications, thanks to collaborations with clinical colleagues. We have established several unique animal models to uncover the mechanisms behind human diseases such as cerebrovascular malformations, acute lung injury, ferroptosis-induced liver fibrosis, obesity-induced diabetes, and acute pancreatitis.