Evgeny Pavlov
New York University, NY·Biochemistry
Mitochondria are the cell's power plants. They make ATP, the cell's energy currency, through oxidative phosphorylation.
- Fields
Biochemistry
Physiology
Biophysics
- Topics
mitochondria
mPT
oxidative phosphorylation
- Grants
- 1 known grant, through Jan 2027
What they work on
- Identify which molecular mechanisms of mitochondrial permeability transition operate under specific stress conditions, such as calcium and reactive oxygen species imbalance, using the lab's animal and cell disease models.
- Measure mPT directly in mitochondrial membranes with the lab's patch-clamp electrophysiology assays to characterize its distinct forms and how each is regulated.
- Connect mitochondrial-level mPT measurements to cell and tissue damage in disease-relevant models to define its role in cell death.
More about the research
The respiratory chain builds up an electrical charge across the mitochondrial inner membrane, and ATP synthase uses that charge to make ATP. For this to work, the inner membrane must stay nearly leak-proof. Under stress, such as calcium overload or excess reactive oxygen species (ROS, damaging oxygen-containing molecules), the membrane can suddenly become leaky. This is the mitochondrial permeability transition (mPT). It collapses the membrane's charge, stops ATP production and can kill the cell. mPT contributes to diseases from heart attack and stroke to neurodegeneration. Blocking it protects tissue, but its molecular basis is poorly understood, so it is not yet a drug target.
Why it matters
mPT causes much of the tissue damage in stroke and heart attack, and it is involved in neurodegeneration. Knowing which molecular pathway drives mPT under which stress could provide a framework for drugs that block it selectively. Such drugs could help protect heart and brain cells from dying.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Elizabeth Jonas
Yale University, CT·Neuroscience
Test whether mice carrying a low-leak mutant ATP synthase c-subunit are protected from delayed hippocampal CA1 neuron death after transient global ischemia induced by two-vessel occlusion in aged animals.
Ryan Boudreau
University of Iowa, IA·Medicine & Clinical Research
Map microRNA binding sites across all genes in nonfailing and failing human hearts using high-throughput methods, to see how miR–target interactions are rewired in heart disease.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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