Aditi Gurkar
University of Pittsburgh, PA·Medicine & Clinical Research
Heart disease becomes more common with age, and environmental insults such as pollutants are thought to speed it up by causing oxidative damage. Oxidative damage is chemical harm from reactive oxygen molecules.
- Fields
Medicine & Clinical Research
Biology
Biomedical Engineering
- Topics
telomeres
telomere damage
oxidative stress
- Grants
- 1 known grant, through Dec 2028
What they work on
- Map how oxidative 8-oxoguanine damage at telomeres signals to mitochondria to drive senescence in human iPSC-derived cardiomyocytes and cardiac fibroblasts, using a light-activated chemoptogenetic tool that damages only telomeres.
- Define how telomere damage in one heart cell type affects neighboring cells and heart electrical activity through released signaling factors, using engineered 3D multicellular heart tissues.
- Examine the molecular role of DNA repair at telomeres in maintaining heart health, by studying how repair of oxidative telomere lesions affects mitochondrial function and senescence in iPSC-derived heart cells.
More about the research
One target of this damage is the telomeres, the protective caps at the ends of chromosomes. Telomeres are usually studied for how they shorten each time a cell divides. Most heart cells rarely divide, though, so shortening cannot explain why the heart ages. This project asks whether oxidative damage at telomeres directly causes early, age-related heart dysfunction, rather than simply appearing alongside it.
Why it matters
Environmental exposures and oxidative stress damage telomeres and are tied to heart disease, but the molecular steps connecting them are unclear. Identifying how telomere damage disrupts mitochondria and drives senescence in heart cells could reveal new therapeutic targets for preventing the progression of cardiac disease, especially disease linked to environmental exposures.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Phillip Yang
Stanford University, CA·Medicine & Clinical Research
Confirm that a cluster of six proteins enriched in mitochondria-rich extracellular vesicles drives the production of new mitochondria, testing their interaction with PGC-1α, the master regulator of mitochondrial biogenesis that is depleted in failing hearts.
Francesca Briganti
University of California-San Diego, CA·Medicine & Clinical Research·Early-career
Test candidate miRNAs in stem-cell-derived heart muscle cells (iPSC-CMs) carrying DCM variants in PLN, RBM20 or TNNT2, to find the mechanisms by which they improve contraction.
Haodi Wu
University of Pittsburgh, PA·Genetics
Define how removing NIPBL changes heart-cell function and gene activity, using human iPSC-derived heart muscle cells with a dTAG degradation switch, functional assays and single-cell RNA sequencing.
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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