Ryan Boudreau
University of Iowa, IA·Medicine & Clinical Research
Heart failure is common, growing, and costly, and it comes with broad changes inside heart cells: genes get switched on and off differently, mitochondria (the cell's energy producers) falter, and ion channels that carry the heart's electrical signals change. This research program pursues three linked projects that ask how these molecular changes, and inherited DNA differences that shape them, drive heart disease.
- Fields
Medicine & Clinical Research
Genetics
Physiology
- Topics
heart failure
cardiomyopathy
arrhythmia
- Grants
- 1 known grant, through Jan 2032
What they work on
- 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.
- Test whether SNPs (single-letter DNA variants) that alter microRNA binding in cardiomyopathy- and arrhythmia-related genes change gene regulation and associate with clinical outcomes in patients.
- Determine whether mitoregulin, a mitochondrial microprotein, protects the heart from ischemia-reperfusion injury by delaying calcium- and ROS-triggered opening of the mitochondrial permeability transition pore or preserving membrane integrity.
- Test whether overexpressing mitoregulin blunts cardiac ischemia-reperfusion injury and heart failure, as a possible new therapeutic approach.
- Define two new regulatory routes controlling SCN5A, the gene for the heart sodium channel NaV1.5, including microRNA-mediated silencing enhanced by a patient SNP.
- Examine roles of NaV1.5 beyond electrical conduction, in heart-cell metabolism and oxidative stress, to learn how lower NaV1.5 levels could worsen heart failure.
More about the research
The first project focuses on microRNAs (miRs), tiny RNA molecules that silence specific genes by binding to their messages. Knowing which genes each miR targets is key to understanding its role, but direct data from real tissue is scarce. The lab uses high-throughput methods to map miR binding sites across the whole set of genes in nonfailing and diseased human hearts. The hypothesis is that heart disease involves rewired miR–target interactions and single-letter DNA variants (SNPs) that disrupt them. The team tests candidate SNP-affected interactions linked to cardiomyopathy (heart muscle disease) and arrhythmia, and checks whether these SNPs relate to patient outcomes.
Why it matters
Heart failure and sudden cardiac death are leading causes of illness and death and cost the US healthcare system over $30 billion a year. Identifying DNA variants that alter microRNA control of heart genes could help flag patients at higher risk, while mitoregulin may offer a new therapeutic avenue to limit damage after heart attacks. Understanding low sodium-channel levels could explain worse outcomes in some heart failure patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Bround
Baylor College of Medicine, TX·Physiology·Early-career
Determine whether LETM1 drives proton/calcium exchange in heart mitochondria, using mice in which Letm1 is deleted from the heart to study heart function, mitochondrial function and how charged particles cross the mitochondrial membrane.
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.
Radhika Muzumdar
University of Pittsburgh, PA·Physiology
Determine how effectively humanin, a small peptide encoded in mitochondria, protects the heart in mouse models of myocardial ischemia-reperfusion injury and ischemia-induced heart failure in aging, measuring infarct size and cardiac function.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
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