Forum Kamdar
University of Minnesota, MN·Biomedical Engineering·Early-career
Duchenne muscular dystrophy (DMD) is the most common and deadly muscular dystrophy. Nearly all patients develop heart muscle disease (cardiomyopathy), and heart failure is now the leading cause of death.
- Fields
Biomedical Engineering
Medicine & Clinical Research
Physiology
- Topics
Duchenne muscular dystrophy
cardiomyopathy
heart failure
- Grants
- 2 known grants, through Apr 2028
What they work on
- Build 3D-bioprinted human chambered muscle pumps (hChaMPs) from DMD patient stem cell-derived heart cells and test how progressively increasing pressure alters mechanotransduction and heart function at early and later disease stages.
- Determine how loss of dystrophin, which links heart cells to the extracellular matrix, changes ECM dynamics and drives cardiac remodeling under volumetric loading.
- Test whether restoring dystrophin early versus late, using precise gene editing or exon skipping, limits contraction-induced injury and rescues function and gene-expression changes in loaded DMD hChaMPs.
More about the research
DMD is caused by mutations in the dystrophin gene. Dystrophin anchors the heart cell's contractile machinery to the surrounding scaffold of proteins, the extracellular matrix (ECM), and spreads mechanical stress across the cell membrane. Without it, heart cells are damaged by their own contractions. There are no effective treatments, partly because existing models do not capture how the human disease progresses. Two linked grants, an early-career research grant and a mentored career-development award, build a 3D human heart model to study how mechanical load drives DMD heart disease and whether restoring dystrophin can halt it.
Why it matters
Boys and young men with Duchenne muscular dystrophy commonly die of heart failure, and no treatment currently prevents or slows this cardiomyopathy. A patient-derived 3D heart model that mimics disease progression could reveal early disease mechanisms. It could also provide a human system for testing dystrophin gene editing and exon skipping. This may help identify disease-specific therapies to prevent DMD cardiomyopathy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
3D Bioprinted Human Model of Duchenne Muscular Dystrophy (DMD) Cardiomyopathy to Study Disease Progression with Imposed Force and Precise Gene Editing
NIH · Jul 2023 – Apr 2028
Progressive loading of a human dystrophic cardiomyopathy 3D model to mimic disease and evaluate therapeutic
NIH · Sep 2022 – Aug 2026
Closest labs
Brenda Ogle
University of Minnesota, MN·Biomedical Engineering
Identify growth factors secreted by epicardial progenitor cells that boost proliferation of hiPSC-derived heart muscle cells, using gene editing and high-throughput proteomics in a 3D-printed layered cardiac tissue.
Joseph Powers
University of Washington, WA·Biophysics·Early-career
Test whether loss of Filamin C (FLNC), a protein linking the heart cell's contractile units to its surroundings, disrupts inside-out force transmission by altering filament lattice geometry in mouse cardiomyocytes, using X-ray diffraction, atomic force microscopy and multiscale modeling.
Renzhi Han
Indiana University-Purdue University-Indianapolis, IN·Pharmacology
Develop an improved triple-vector system in next-generation myotropic adeno-associated virus capsids to reconstitute full-length dystrophin by protein trans-splicing across skeletal, diaphragm, and heart muscle in models of Duchenne muscular dystrophy.
The school
University of Minnesota: 88 labs on PI Pages, $1.4B a year on research, 722 research doctorates a year.
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