Sin-Jin earned her Ph.D. in Animal Science and Technology from the National Taiwan University (NTU), focusing on investigating the role of mitochondria in obesity cardiomyopathy using the Lee-Sung minipig model. Prior to this, she served as a postdoctoral fellow at Academia Sinica, delving into the mechanism of adipose CPEB2 in promoting the synthesis of beneficial brown adipose tissue adipokines, directly or indirectly, to safeguard cardiac function following trans-aortic banding surgery.

Following this stint, she joined Dr. Bereketeab Haileselassie's lab to further her research at Stanford University, delving into the mechanisms of extracellular mitochondria in cardiomyopathy through lipotoxicity induction, both in vitro and in vivo. Additionally, she explored the contribution of damaged extracellular mitochondria to immune dysregulation and end-organ failure.

Currently, she serves as an assistant professor in the Bachelor Program of Biotechnology and Food Nutrition at NTU, where she continues her research in mitochondrial biology in metabolic-related diseases. Outside the lab, she enjoys various ball sports, scuba diving, and traveling.

Research Expertise: Mitochondrial Biology / Lipid Metabolism / Animal Nutrition / Metabolic Syndrome

Obesity is associated with many diseases, including type 2 diabetes (T2DM), hepatic steatosis and cardiovascular disease (CVD). Mitochondrial dynamics, a process of biogenesis, fusion, fission and mitophagy determines mitochondrial morphology, quality and functions. These mitochondrial properties are essential for maintaining healthy mitochondrial networks. Latest studies suggest that these alterations in mitochondrial fission and mitophagy result in the release of damaged extracellular mitochondria (exMito) and associated byproducts that have been shown to induce an inflammatory response in neurodegeneration diseases and sepsis-induced cardiomyopathy models. Furthermore, inhibition of DRP1/Fis1 dependent mitochondrial fission by a rationally designed peptide (P110) may have neuroprotective impact by decreasing the amount of damaged extracellular mitochondria (exMito) released. However, the exact role of this mechanism on metabolic diseases has not been adequately explored.

We welcome any students interested in mitochondrial biology and metabolic-related diseases; please contact us for potential opportunities to join our lab : )