Molecular Signaling of Human Diseases

External stressors have to confer pathological effect through specific intracellular signal transduction networks. Although much of the stress mediated signaling events are designed to induce compensatory changes in hearts in order to sustain the initial insults, prolonged or abnormal stresses promote the progression of the disease by inducing maladaptive remodeling. Uncovering the molecular and cellular mechanisms of stress-activated signaling pathways in human diseases constitutes the main interest of our laboratory.

Current research program evolves around the following three broad but integrated areas:

1. Molecular signaling in mitochondrial function and regulation. We have developed state-of-the-art experimental tools to investigate the fundamental basis of mitochondrial function and regulation. Particularly, we are focusing on mitochondria mediated non-apoptotic cell death and metabolic regulation via intra-mitochondrial signaling pathways.

2. ER stress signaling in cellular physiology and human diseases. We are studying novel regulatory components in ER stress signaling pathway and its impact on physiological vs. pathological ER stress response in human diseases, such as heart failure and metabolic defects.

3. Amino acids mediated signaling in the regulation of cell death and growth. This is an emerging research area with significant implications in many human diseases, including degenerative diseases and cancer.

Source:  https://www.uclaaccess.ucla.edu/Faculty.aspx?rv_FacultyId=3555