Dmitry A Terentyev
Ohio State University, OH·Physiology
Sudden cardiac death from dangerous fast heart rhythms triggered by stress is a leading cause of death worldwide. In heart muscle cells, calcium signals that drive each heartbeat are tightly linked to how mitochondria, the cell's power plants, make energy.
- Fields
Physiology
Medicine & Clinical Research
Biophysics
- Topics
cardiac arrhythmia
ventricular tachycardia
sudden cardiac death
- Grants
- 1 known grant, through May 2027
What they work on
- Test whether overactive RyR2, the heart's calcium-release channel, activates calpain, a calcium-activated enzyme inside mitochondria, which then breaks down OPA1, a protein that shapes mitochondrial inner folds, using a rat model of CPVT the lab created.
- Determine whether reduced COX7RP, a protein that helps assemble energy-making supercomplexes, causes faulty mitochondrial electron transport and excess ROS in hypertrophic and failing hearts, worsening abnormal calcium handling.
- Examine sex differences in mitochondrial function linked to higher COX7RP and OPA1 levels in healthy female versus male heart muscle cells.
More about the research
This link is called excitation-contraction-bioenergetics coupling. Under stress, more calcium enters mitochondria and speeds energy production. But this also raises the risk of producing reactive oxygen species (ROS), damaging forms of oxygen. Too much ROS can harm the calcium-handling machinery, including the ryanodine receptor (RyR2), the channel that releases calcium inside the cell. This can trigger arrhythmias.
Why it matters
Dangerous heart rhythms in inherited syndromes and in acquired disease such as heart failure can lead to sudden death. Identifying molecular targets that break the cycle between faulty calcium signaling and mitochondrial dysfunction could point to therapies that reduce arrhythmias and improve how well the heart pumps.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Martin Morad
University of South Carolina-Columbia, SC·Physiology
Compare calcium-signaling defects caused by CPVT1 mutations in different regulatory regions of the cardiac calcium-release channel RyR2 in maturated human iPSC-derived heart cells, reverse them by editing the sequence back, and test drug responses.
Shey-Shing Sheu
Thomas Jefferson University, PA·Physiology
Test whether hypertrophic stress raises levels of mitochondrial ryanodine receptor type 1 (mRyR1), a calcium channel, to boost mitochondrial calcium uptake and ATP production, using RyR1-overexpressing and other mouse models.
Steven Marx
Columbia University, NY·Physiology
Determine how β-adrenergic stimulation of the CaV1.2 calcium channel changes in heart failure, using knock-in mice whose Rad brake protein cannot be phosphorylated by protein kinase A and mice lacking the Rad–beta-subunit interaction.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
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