Qing Miao, PhD

My 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 that I identified during my postdoctoral training at Yale School of Medicine. Our ongoing work at the Medical College of Wisconsin has shown 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 host resilience.

Resilience refers to 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, which is crucial for preventing T2D. Additionally, our research indicates that hyperglycemia in diabetes patients may reduce vascular resilience, leading to 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 molecular mechanisms behind human diseases such as cerebrovascular malformations, acute lung injury, nonalcoholic fatty liver disease, lipid peroxidation-caused liver injury, and obesity-induced diabetes.