Phillip Yang
Stanford University, CA·Medicine & Clinical Research
A failing heart is, among other things, an energy-starved heart. Heart muscle burns enormous amounts of fuel, and in hypertrophic, dilated and ischemic cardiomyopathy the mitochondria — the structures that generate the cell's chemical energy currency, ATP — are visibly damaged and produce less of it even as demand rises.
- Fields
Medicine & Clinical Research
Physiology
Biomedical Engineering
- Topics
heart failure
cardiomyopathy
extracellular vesicles
- Grants
- 1 known grant, through Mar 2027
What they work on
- 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.
- Determine how mitochondria-rich extracellular vesicles protect heart muscle cells derived from induced pluripotent stem cells in a laboratory model of oxygen deprivation, tracing the route from mitochondrial transfer to restored ATP production.
- Assess whether augmenting mitochondria and stimulating their production improves cardiac function in a mouse model of chronic myocardial injury, measuring functional benefit after vesicle delivery.
- Test how the vesicle protein cluster alters the heart cell's main energy pathways — oxidative phosphorylation, fatty acid metabolism and glycolysis — to establish the bioenergetic mechanism behind tissue repair.
More about the research
Current heart failure treatments do not address this energy shortfall directly, and this project tests whether it can be corrected by delivering working mitochondria and the machinery to make more of them.
Why it matters
Heart failure carries high mortality and remains incompletely treated, in part because current therapies do not address the mismatch between the energy a failing heart needs and what it can produce. Mitochondria-rich extracellular vesicles secreted by stem-cell-derived heart cells could offer a cell-free alternative to cell transplantation — avoiding arrhythmia, tumor risk and graft failure — that restores energy production in injured heart muscle.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
Aditi Gurkar
University of Pittsburgh, PA·Medicine & Clinical Research
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.
The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
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