My Research Interests:
I have long-standing research interests in diabetes research. My research work mainly focuses on novel signal transduction pathways that regulate glucose-sensing of pancreatic β-cells. This is an important area of research, since a loss of glucose responsiveness of pancreatic β-cells plays a pivotal role in the development of type 2 diabetes. However, molecular mechanisms underlying the causes of defective glucose-sensing of islet β-cells in type 2 diabetes remains poorly understood.
Why I Pursued Aging Research:
I believe aging is one of the last frontiers of life sciences, since we still do not know much how we get old and how aging kills us through the deployment of various metabolic diseases, such as diabetes, obesity, cardiovascular diseases, cancer, and neurodegenerative diseases. Although this age-old problem has forever baffled humans, I am confident that we will concur this problem someday, which inspires me to be involved in aging research.
My Future Plans:
Aging significantly deteriorates islet β-cell function, leading to increased risk of T2DM. Islet β-cells are particularly sensitive to oxidative stress and mitochondrial dysfunction associated with aging, since redox signaling plays a pivotal role in glucose-stimulated insulin secretion. Additionally, ATP production from mitochondrial oxidative phosphorylation is the primary driving force for glucose-stimulated insulin secretion by triggering the closure of ATP sensitive potassium channel. Hence, oxidative stress and mitochondrial dysfunction are implicated in the pathogenesis of islet β-cell failure of T2DM, as evidenced by decreased expression of mitochondrial genes, disruption of mitochondrial network, and mitochondrial swelling in T2DM. My future plans will focus on how mitochondrial regulates glucose-stimulated insulin section in islet β-cell during aging.
Awards and Honors:
- 2015 NIA T32 Biology of Aging Training Grant
- 2014 Outstanding PhD Student Award of Jiangsu Province, Nanjing, China
- 2013 Excellent Doctoral Dissertation of Nanjing Medical University, Nanjing, China
- 2012 First Place of Best Oral Presentation Awards, 5th Annual Conference of Midwest Islet Cell Club, University of Pittsburgh, PA, USA
- 2011 Career Award, 4th Scientific Symposium of the Chinese American Diabetes Association (CADA), San Diego, CA, USA
- 2010 Best Poster Award, 7th Diabetes and Obesity Research Symposium, Penn State University College of Medicine, Hershey, PA, USA
Wang L, Liu X, Nie J, Zhang J, Kimball SR, Zhang H, Zhang WJ, Jefferson LS, Cheng Z, Ji Q, Shi Y. (2015) ALCAT1 controls mitochondrial etiology of fatty liver diseases, linking defective mitophagy to steatosis. Hepatology. 2015 Feb; 61(2):486-96.
Zhang J, Xu D, Nie J, Han R, Zhai Y, Shi Y. (2014) Comparative gene identification-58 (CGI-58) promotes autophagy as a putative lysophosphatidylglycerol acyltransferase. J Biol Chem. 289(47):33044-53.
Zhang J, Xu D, Nie J, Cao J, Zhai Y, Tong D, Shi Y. (2014) Monoacylglycerol acyltransferase-2 is a tetrameric enzyme that selectively heterodimerizes with diacylglycerol acyltransferase-1. J Biol Chem. 289(15):10909-18.
Nie J, Han X, Shi Y. (2013) SAD-A and AMPK kinases: the "yin and yang" regulators of mTORC1 signaling in pancreatic β cells. Cell Cycle. 12(21):3366-9.
Nie J, Liu X, Lilley BN, Zhang H, Pan YA, Kimball SR, Zhang J, Zhang W, Wang L, Jefferson LS, Sanes JR, Han X, Shi Y. SAD-A kinase controls islet β-cell size and function as a mediator of mTORC1 signaling. Proc Natl Acad Sci U S A. 110(34):13857-62