Jeffrey R Martens, Ph.D.

The Martens Lab is focused in two areas of Pharmacology and Therapeutics, including sensory Neuropharmacology and cardiovascular Pharmacology, with work in both the heart and olfactory systems.

In relation to the olfactory system, the lab’s work is devoted to understanding mechanisms of olfaction, pathogenesis of olfactory dysfunction, and the development of curative therapies for anosmia. Olfactory dysfunction in the general population is frequent, affecting at least 2.5 million people in the U.S. alone. In at least 20% of the cases, the etiology of the chemosensory disturbance cannot be identified. The Martens Lab was one of the first to demonstrate olfactory dysfunction as a clinical manifestation of an emerging class of human genetic disorders, termed ciliopathies, which involve defects in ciliary assembly, maintenance, and/or function. Most importantly, the lab has demonstrated that gene therapy can be used to successfully rescue anosmia resulting from the malformation/loss of cilia. Projects in the laboratory seek to identify direct mechanisms by which sensory input and deprivation regulate olfactory function and to learn how these are disrupted in disease states. Specifically, they work to elucidate the mechanisms underlying the transport of odorant signaling proteins into cilia of olfactory sensory neurons and their alterations in cilia-related disorders. In addition, work completed in the laboratory seeks to understand the importance of cilia for neurogenesis and cell differentiation, investigating their contribution to the regenerative properties of olfactory basal stem cells. Together, this work contributes to the understanding of the pathogenesis of human sensory perception diseases and paves the way for the development of treatments for olfactory loss in humans, where no curative therapies for ciliopathic disease exist.

In relation to the cardiovascular system, projects in the Martens Lab are focused on the identification of novel targets for the treatment of cardiac arrhythmias. In particular, the lab is interested in therapies for atrial fibrillation, which is the most common cardiac arrhythmia, affecting more than 2 million Americans. This electrical instability in the human heart can occur through a primary genetic defect in ion channel function or an acquired disorder attributable to ion channel dysregulation. They are interested in the regulation of voltage-gated potassium (Kv) channels that are vital for atrial repolarization in the human heart. Work in their laboratory is devoted to understanding the details of Kv channel regulation, trafficking, and pharmacological modulation and to learning how this is all integrated into the broader context of normal cardiomyocyte signaling and the pathogenesis of disease.