Eduardo S. Fricovsky, PharmD

Research Summary

Dr. Fricovsky’s research interest includes diabetic cardiomyopathy and the effects of enzymatic protein glycosylation (O-GlcNAc) in type 2 diabetic mouse hearts and their influence on cardiac function. Also, conducts studies related to the expression of O-GlcNAcase (GCA) an enzyme that removes excessive O-GlcNAc modification and protection against diabetic cardiomyopathy. Furthermore, he examines the role of GCA gene expression and O- GlcNAc levels in non-diabetics and diabetic patients at the UC San Diego Student-Run Free Clinic.

Academic Achievements

Education: B.S. in Biochemistry/Chemistry (2002) UC San Diego; UCSF School of Pharmacy (2006); NIH T32 Research Fellow (2006-2009) UC San Diego, Department of Medicine.

Awards and Honors: ASHP Outstanding Professional Development Project Award (2014); American Pharmacy Association National Immunization Champion Award (2014); UC San Diego Student Run Free Clinics Community Leadership Award (2013); UC San Diego Health Science Academic Senate Research Award (2012) UC San Diego Student Run Free Clinic Angel Award (2012); Society of Chemical Industry Teacher Award (2011); UC San Diego Skaggs School of Pharmacy Excellence in Teaching Award (2009-2010); UC San Diego Student Run Free Clinic Project Clinical Leader Award (2009); UC San Diego Student Run Free Clinic Project Pharmacy Faculty Leader Award (2008).

Leadership Experience: Founder and President of the UCSF Latino Association of Pharmacy Students (LAPS) (2003- 2005); UC San Diego Student Run Free Clinic Project Pharmacy Director (2009-Present); AdHoc SSPPS Non-Salary Faculty Review Committee (2009- Present); Co-Chair SSPPS ACTION Academic Communities (2010-Present); UC San Diego OASIS Alumni Committee Officer (2012-Present)

Teaching

• Pharmacy Therapeutics (SPPS 212A).
• Pharmacy Practice (SPPS 201, 202, 203).
• Pharmacy Preceptor: UC San Diego Student-Run Free Clinic Project (IPPE & APPE).

Selected Publications

• Suarez et al. (2008). Alterations in mitochondrial function and cytosolic calcium induced by hyperglycemia are restored by mitochondrial transcription factor A in cardio-myocytes. Am J Physiol Cell Physiol. 295:C1561-C1568.
• *Romero-Perez et al. (2008). Cardiac uptake of minocycline and mechanisms for in vivo cardioprotection. J Am Col Cardiol. 52:1086-1094.
  * Shared first co-First Author.
• Hu et al. (2009). Increased enzymatic O- GlcNAcylation of mitochondrial proteins impairs mitochondrial function in cardiac myocytes exposed to high glucose. J Biol Chem. 284:547-555.
• Griffin et al. (2010). Tetracyclines: a pleitropic family of compounds with promising therapeutic properties. Review of the literature.Am J Physiol Cell Physiol.
• Fricovsky et al. (2012). Excess protein O- GlcNAcylation and the progression of diabetic cardiomyopathy. Am J Physiol Regul Integr Comp Physiol. 303:R689-99
• Suarez et al. (2013). Sorcin modulates mitochondrial Ca2+ handling and reduces apoptosis in neonatal rat cardiac myocytes. Am J Physiol Cell Physiol. 304:C248-56.
• *Aguilar et al. (2014). Role for high glucose induced protein O-GlcNAcylation in stimulating cardiac fibroblast collagen synthesis.Am J Physiol Cell Physiol. 306(9):C794-804.
  * Shared first co-First Author.

View on PubMed