Victor MALTSEV

Title: Senior Associate Scientist

Office(s): Cellular Biophysics Section (CBPS)

Phone Number: 410-558-8426

Email Address: maltsevvi@mail.nih.gov

Biography

I got my master’s degree in biophysics in 1982 at Moscow Institute of Physics and Technology and Ph.D. in Biological Sciences in 1991. After postdoctoral studies of cardiac differentiation of embryonic stem cells at the Free University of Berlin, I worked as Staff Investigator at Henry Ford Health System in Detroit studying cellular mechanisms of cardiac arrhythmias. I joined Laboratory of Cardiovascular Science in 2002 as Staff Scientist and my research has been focused on biophysical mechanisms of heart rate regulation and its deterioration with age. Together with my LCS colleagues we discovered a new mechanism of cardiac impulse initiation that involves intracellular calcium oscillator (dubbed calcium clock) coupled to a membrane oscillator (membrane clock). Together with Edward Lakatta we created the first numerical model of the coupled clock pacemaker system that explained numerous experimental data. Components of both clocks interact via explosive positive feedback mechanisms, so-called ignition process that insures robustness of cardiac impulse initiation. We further considered cardiac pacemaking is an emergent property of complex synchronized signaling on multiple scales. At the lowest scale heart beat depends on individual molecules synchronizing their states to generate robust intracellular signals over the thermal noise. We discovered that this first emerging level of heartbeat is achieved via synchronized openings and closings of calcium release channels that is mathematically described as the phase transition associated with spontaneous magnetization (so called ordered spin state). We further discovered that calcium release system also exhibits order-disorder phase transitions linked to abnormal “leaky” releases. We hypothesize that cardiac rhythm deterioration with age is due, in part to disordered operation of the release channels over their synchronized (“magnetized”) action. Other aging-associated changes include deterioration of signal synchronization at higher scales, including interactions of local calcium releases with membrane ion channels and interactions among cells within the pacemaker tissue.

For a full list of publications by Victor Maltsev, click here.