Yuriy Usachev, PhD

Contact Information

Office: 2-340F BSB 
Phone: 319-335-9388 
Faculty Profile

Brief description of current research:

Our research focuses on the roles of mitochondria in regulating neuronal plasticity and survival under conditions of stress or illness, such as hyperglycemia in diabetes. In particular, we are trying to understand how impairment of mitochondrial function contributes to the pathogenesis of peripheral diabetic neuropathy (PDN), which is one of the most common complications of diabetes affecting more than 50% of 20 million diabetes patients in North America and leading to either severe neuropathic pain or sensory loss. We also explore novel approaches to prevent or treat PDN. We use a multidisciplinary approach in our research that involves genetic and molecular tools combined with patch-clamp electrophysiology and fluorescent microscopy, as well animal models of diabetes. Our recent data using animal model of diabetes suggest that phosphorylation-dependent enhancement of mitochondrial fusion in sensory neurons provides remarkable protection from diabetes-induced sensory loss. We anticipate that identifying mechanisms responsible for mitochondrial fusion-dependent neuroprotection in PDN, and developing therapeutic strategies targeting this process to prevent or slow progression of PDN will be major breakthroughs in the field of diabetes research.


3 most influential diabetes/obesity/metabolism publications:

  • Medvedeva Y.V., Kim M.-S. and Usachev Y.M.:  Mechanisms of prolonged presynaptic Ca2+ signaling and glutamate release induced by TRPV1 activation in rat sensory neurons. Journal of Neuroscience 28:5295-5311, 2008. **This article was featured in the “This week in the journal” section. It was also highlighted in EurekAlert, an online global news service operated by AAAS (American Academy of Arts and Science), and selected for Faculty of 1000 Biology.
  • Kim M.-S. and Usachev Y.M.:  Mitochondrial Ca2+ cycling facilitates activation of the transcription factor NFAT in sensory neurons. Journal of Neuroscience 29:12101-12114, 2009.
  • Shutov, L.P., Kim M.-S., Houlihan P.R., Medvedeva Y.V. and Usachev Y.M.:  Mitochondria and plasma membrane Ca2+ -ATPase (PMCA) control presynaptic clearance in capsaicin-sensitive rat sensory neurons. Journal of Physiology, 591: 2443-2462, 2013. **This article acknowledges support by UI FOEDRC



What has captured my interest in research on diabetes and peripheral diabetic neuropathy is the enormousness of the problem, patients’ suffering and the lack of disease-modifying treatments. Indeed, according to the American Diabetes Association, 25.8 million Americans have diabetes, and approximately 50% of these patients have peripheral diabetic neuropathy (PDN), which is the most common complication of diabetes. More than 30% of patients with PDN suffer from severe chronic (neuropathic) pain, whereas the rest develops sensory loss, which may ultimately lead to gangrene and limb amputation. Thus, disease modifying treatments are desperately needed for PDN.

Another aspect that makes me so interested in diabetes is that it is a very complex multifaceted disorder that involves malfunction of many mechanisms and signaling pathways throughout the body, making diabetes and PDN a very interesting and challenging scientific problem. We are trying to bring our expertise in neuroscience, sensory biology and mitochondrial function into this relatively new area of research for our lab to better understand the mechanisms that lead to sensory axon degeneration in PDN and to identify new targets and strategies to treat PDN.