Radhika Muzumdar
University of Pittsburgh, PA·Physiology
A heart attack does damage in two stages. Blood flow is cut off, starving heart muscle of oxygen, and then restoring that flow causes a second wave of injury as metabolism lurches and reactive oxygen species, chemically aggressive byproducts of oxygen use, accumulate.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
humanin
mitochondrial peptide
cardioprotection
- Grants
- 1 known grant, through May 2027
What they work on
- 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.
- Test whether humanin's protection works by shifting heart muscle cell metabolism toward peroxisomal fatty acid oxidation while inhibiting mitochondrial fatty acid oxidation, using primary cardiomyocytes and heart lysates.
- Establish whether humanin lowers reactive oxygen species and improves cardiomyocyte survival after low oxygen and oxidative stress, linking these effects to reduced acute heart muscle cell death.
- Measure humanin levels in heart tissue and circulation of human subjects with post-ischemic cardiac failure, as an exploratory test of whether the peptide tracks with human disease.
More about the research
Together these drive heart muscle cell death and the slide toward heart failure. Age makes all of this worse, and coronary artery disease remains a leading cause of death worldwide. This project tests whether a small peptide made by mitochondria, the cell's energy-producing compartments, can shield the aging heart through that injury sequence.
Why it matters
Coronary artery disease causes major illness and death worldwide, and older patients fare worst after a heart attack. If humanin protects heart muscle during blockage and reperfusion and prevents the drift into heart failure, it could become a treatment option for acute myocardial infarction in the elderly; measuring humanin in patient heart tissue and blood may also indicate whether the peptide is relevant to human post-ischemic heart failure.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jidong Fu
Ohio State University, OH·Medicine & Clinical Research
Characterize how Masir, a membrane-associated long noncoding RNA, protects heart muscle cells from ischemic injury by enhancing membrane repair, and assess its safety in mouse models.
Lai-Hua Xie
Rutgers University-New Brunswick, NJ·Physiology
Determine whether the mitochondrial calcium uniporter (mCU), a channel admitting calcium into mitochondria, also carries iron into heart-cell mitochondria and drives calcium dysregulation, oxidative stress and iron-induced cardiac toxicity, in isolated myocytes and in vivo.
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
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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