Sangkyun Cho
Johns Hopkins University, MD·Biomedical Engineering·Early-career
When the heart is injured or overworked, it lays down stiff scar tissue. That scarring, called fibrosis, shows up in nearly every form of heart disease, from inherited cardiomyopathies to heart failure after a blocked artery, and there is no effective drug to reverse it.
- Fields
Biomedical Engineering
Physiology
Medicine & Clinical Research
- Topics
cardiac fibrosis
myofibroblast
cardiac fibroblast
- Grants
- 1 known grant, through Jul 2028
What they work on
- Test in real time whether releasing mechanical load drives cardiac myofibroblasts back toward a quiescent state, using iPSC-derived fibroblast reporter lines with fluorescently tagged marker genes such as CFP-TAGLN in a dynamically softening hydrogel.
- Determine how matrix stiffness and TGF-beta signaling interact to set myofibroblast states, by mapping stiffness-dependent protein interactions of mechanosensitive transcription factors including YAP.
- Identify epigenetic regulators acting downstream of matrix stiffness in cardiac fibroblasts using single-cell ATAC sequencing, which maps regions of DNA that are open for transcription.
- Find druggable targets within the cell's mechanosensing machinery and test candidate compounds in engineered heart tissues and in a mouse model of pressure-overload hypertrophy and heart failure.
More about the research
Much is known about the signals that first wake up quiet cardiac fibroblasts and turn them into myofibroblasts, the contractile, matrix-producing cells that build scar. Far less is known about why those myofibroblasts stick around for years. This project asks whether the physical stiffness of a cell's surroundings is what locks them in that state, and whether softening those surroundings can let them revert.
Why it matters
Cardiac fibrosis contributes to illness and death across essentially all cardiovascular disease, yet no therapy reverses it. Showing that myofibroblasts can be coaxed back toward a quiet state by changing mechanical signaling, and identifying specific proteins in that pathway that drugs can hit, could open a route to anti-fibrotic treatments for patients with heart failure and cardiomyopathy.
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.
Michael Blatchley
Syracuse University, NY·Biomedical Engineering·Early-career
Test how light-triggered softening or stiffening of a PEG hydrogel matrix changes the cell-type makeup and maturation of iPSC-derived intestinal epithelial organoids over time.
Michael Kapiloff
Stanford University, CA·Physiology
Define how phospholamban bound to AKAP6β at the outer nuclear membrane regulates calcium efflux from a nanometer-scale perinuclear compartment and myocyte growth, using live-cell imaging and biochemical assays in rat ventricular myocytes and human stem cell-derived cardiomyocytes.
The school
Johns Hopkins University: 100 labs on PI Pages, $4.1B a year on research, 622 research doctorates a year.
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