Peng Yao
University of Rochester, NY·Physiology
Heart disease is the leading cause of death worldwide. Heart muscle cells need a steady energy supply and tight control over which proteins they make.
- Fields
Physiology
Biochemistry
Medicine & Clinical Research
- Topics
cardiomyocyte
heart failure
myocardial infarction
- Grants
- 2 known grants, through Jun 2027
What they work on
- Determine how FAM210A regulates mitochondrial calcium balance, testing whether it acts as a regulator of the calcium/proton exchanger LETM1 in cardiomyocytes, in vitro and in vivo.
- Define the role of FAM210A in cardiac mitochondrial respiration and heart function using cardiomyocyte-specific Fam210a knockout mice, including how the integrated stress response drives disease.
- Test whether AAV9-delivered FAM210A overexpression protects mitochondria, cardiomyocytes and heart function in mouse models of myocardial infarction.
- Map the mRNA structural elements, such as double-stranded RNA unwound by the helicase DDX3X, that work with the GATA4 uORF to control how much GATA4 protein is made.
- Determine the biological role of the GATA4 uORF in cardiac hypertrophy using CRISPR-Cas9 start-codon knock-in mice and primary cardiomyocyte cultures, at baseline and under stress.
- Develop proof-of-concept antisense oligonucleotides that lock or disrupt the uORF RNA structure to tune GATA4 translation and reduce pathological heart enlargement.
More about the research
When either fails, the heart can weaken or thicken abnormally. The lab's two projects examine these processes in heart muscle cells, called cardiomyocytes. One focuses on how mitochondria, the cell's energy factories, manage calcium. The other focuses on how protein production is controlled at the level of messenger RNA (mRNA). Both look for new targets for treating heart disease.
Why it matters
Patients with mitochondrial cardiomyopathy, heart attack and ischemic heart failure could benefit if FAM210A proves to be a useful therapeutic target, for example through gene delivery that raises its levels. For pathological cardiac hypertrophy, RNA-based drugs that adjust GATA4 protein production may offer a new treatment approach. The same ASO design strategy could be applied to other disease-causing mRNAs.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xiaolei Liu
Temple University, PA·Physiology
Determine the molecular pathways and targets through which lymphatic growth in the heart improves cardiomyocyte survival after myocardial infarction, building on survival signals such as Reelin released by lymphatic endothelial cells.
Frank Conlon
University of North Carolina at Chapel Hill, NC·Genetics
Test whether DDX3X, an X-linked RNA helicase that escapes X-inactivation, regulates sex-specific mRNA translation in heart muscle cells, using a conditional Ddx3x mouse allele.
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 Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.
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