Skaggs School of Pharmacy and Pharmaceutical Sciences
Department of Pharmacology, School of Medicine
Dr. Gustafsson is interested in understanding the molecular pathways that regulate the life and death of cardiac myocytes. The occurrence of cardiovascular disease increases with advancing age and intrinsic alterations in aging cardiac myocytes are a major contributor to the underlying pathogenesis. In particular, a decline in mitochondrial function is considered to play a key role in the increased susceptibility to disease. In the heart, the primary function of mitochondria is to meet the high energy demand of the beating myocytes by providing ATP through oxidative phosphorylation. Mitochondrial dysfunction and activation of cell death pathways are common occurrences in cardiovascular disease and contributes to the development of heart failure. Dr. Gustafsson uses genetic, cell and molecular biology approaches, mouse models, and cutting-edge 2D/3D imaging techniques to study the signaling pathways involved in regulating mitochondrial structure, function, and turnover in cells and heart. Specifically, Dr. Gustafsson's research is examining how the E3 ubiquitin ligase Parkin regulates removal of dysfunctional mitochondria in cells; and b) determining the molecular mechanisms by which BCL-2 family proteins regulate mitochondrial function, morphology and turnover in cells.
B.S. in Molecular Biology (1996) UCSD; Ph.D. in Biomedical Sciences, Dept. of Pharmacology (2001) UCSD; Postdoctoral Fellowship (2005) Scripps Research Institute.
Awards and Honors:
Elected Fellow of the International Society for Heart Research (2016); ISHR Outstanding Investigator Award (2014); AHA Established Investigator Award (2014); Elected Fellow of the American Heart Association (2010); Keith and Eva Killam Memorial Award, Western Pharmacological Society (2010); AHA BCVS Outstanding Early-Career Investigator Award Finalist (2008); AHA Scientist Development Grant (2007); Young Investigator Award Winner, International Society for Heart Research American Section (2005); TRDRP New Investigator Award (2005);
Chair Biomedical Sciences Graduate Program; Co-Chair of Keystone Meeting (2017; AHA BCVS Leadership Committee member; Chair AHA BCVS Marcus Award Committee, Co-Chair 2015 AHA BCVS Meeting; ISHR Council member; ISHR Executive Committee member; ISHR Treasurer.
- Principles of Pharmacology & Physiology (SPPS 247).
- Contemporary Topics in Pharmacology (SPPS 218B).
- Identified a novel mechanism of eliminating dysfunction mitochondria in cells.
- Elucidated the importance of autophagy in removing damaged mitochondrial in cardiac cells.
- Discovered key roles for mitophagy and mitochondrial remodeling during differentiation of progenitor cells.
- Woodall, B.P et al. (2019) Parkin Does Not Prevent Accelerated Cardiac Aging in Mitochondrial DNA Mutator Mice. JCI Insight. 4(10):e127713
- Lampert, M.A., et al. (2019) BNIP3L/NIX and Fundc1-Mediated Programmed Mitophagy is Required for Mitochondrial Network Remodeling during Cardiac Progenitor Cell Differentiation. Autophagy 15(7): 1182-1198
- Shires, S.E., et al. (2020) Nuclear Parkin Activates the ERRα Transcriptional Program and Drives Widespread Changes in Gene Expression Following Hypoxia. Scientific Reports 10:8499.
- Liang, W., et al. (2020) Aging is associated with a decline in Atg9b-mediated autophagosome formation and appearance of enlarged mitochondria in the heart. Aging Cell 19(8):e13187
- Hammerling, B.C. et al. (2017) A Rab5 Endosomal Pathway Mediates Parkin-Dependent Mitochondrial Clearance. Nat. Comm. 8:14050
- Expertise in mitochondrial function and cell death signaling pathways in cardiac cells.
- Broad array of molecular and cellular laboratory techniques and in vivo mouse models of heart failure.