Congcong He, PhD



Congcong He, PhD


Assistant Professor


Office Phone



Cell and Molecular Biology


Tarry 8-767


Areas of Research

Cell Biology, Mechanisms of Drug Action, Molecular Neuroscience, Neurobiology of Disease

NU Scholar Profile

Current Research

Current Research

My research focuses on the roles and mechanisms of autophagy in metabolic and behavioral regulation and in pathogenesis of related disorders, such as obesity and type 2 diabetes, neurodegeneration, and tolerance and dependence to psychoactive drugs. Autophagy is a lysosomal degradation pathway essential for nutrient recycling, cellular maintenance and physiological function. Autophagy is intensely induced by physiological stimuli or stress, such as starvation and physical exercise, and malfunction of autophagy has been implicated in a variety of diseases, including neurodegeneration, cardiovascular diseases, cancer and metabolic disorders. There are currently three major directions of study in my laboratory: 1) autophagy in preventing drug tolerance and dependence; 2) the role of autophagy genes in neurodegeneration; and 3) the mechanism of autophagy in mediating exercise-induced metabolic benefits.

Selected Publications

Selected Publications

1. Rocchi A and He C. (2015). Emerging roles of autophagy in metabolism and metabolic disorders. Frontiers in Biology. 10 (2). 154-64.

2. Zhang W and He C. (2014). Regulation of plasma membrane receptors by a new autophagy-related Beclin family member. Autophagy. 10 (8). 1472-3.

3. He C, Wei Y, Sun K, Li B, Dong X, Zou Z, Liu Y, Kinch LN, Khan S, Sinha S, Xavier RJ, Grishin NV, Xiao G, Eskelinen E-L, Scherer PE, Whistler JL and Levine B. (2013). Beclin 2 functions in autophagy, degradation of G protein-coupled receptors, and metabolism. Cell. 154 (5). 1085-99.

4. He C, Bassik MC, Moresi V, Sun K, Wei Y, Zou Z, An Z, Loh J, Fisher J, Sun Q, Korsmeyer S, Packer M, May HI, Hill JA, Virgin HW, Gilpin C, Xiao G, Bassel-Duby R, Scherer PE and Levine B. (2012). Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis. Nature. 481, 511-5.

5. He C and Klionsky DJ. (2006). Autophagy and neurodegeneration. ACS Chemical Biology. 1 (4), 211–3.