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Joseph Powers

University of Washington, WA·Biophysics·Early-career

Dilated cardiomyopathy (DCM) is a common and deadly inherited heart disease. In DCM, the heart's main pumping chamber enlarges and contracts weakly.

Fields

Biophysics

Physiology

Biomedical Engineering

Topics

dilated cardiomyopathy

Filamin C

cardiomyocytes

Grants
1 known grant, last ended Aug 2026

What they work on

  1. 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.
  2. Apply X-ray diffraction, atomic force microscopy and modeling to a human dilated cardiomyopathy model: heart cells derived from gene-edited induced pluripotent stem cells carrying a patient-specific FLNC-truncating variant.
  3. Test whether truncated FLNC disrupts outside-in mechanosignaling and promotes harmful remodeling in human stem-cell-derived heart cells, using FRET-based molecular tension sensors, mechanical loading and transcriptomics of hypertrophy genes.

More about the research

It is often caused by mutations in proteins that form the internal scaffolding of heart muscle cells (cardiomyocytes). Current treatments only slow the disease. A key idea is that these mutations disrupt how heart cells sense and pass along mechanical forces. That includes the forces the cell's own contractile machinery generates and the forces it feels from its surroundings. These force-sensing pathways may drive harmful remodeling of the heart.

Why it matters

Patients with dilated cardiomyopathy currently have treatments that only delay disease progression. By revealing how defects in Filamin C disrupt force sensing and force transmission in heart cells, this work could identify mechanisms to target with new treatments. Such treatments could prevent or slow mechanically triggered harmful remodeling of the heart.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Dysregulated mechanosignaling in dilated cardiomyopathy caused by defective Filamin C

NIH · Sep 2023 – Aug 2026

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.

Ryan Stowers

University of California-Santa Barbara, CA·Biomedical Engineering

Determine whether cardiomyopathy-driven remodeling of the extracellular matrix alters myocardial viscoelasticity, by mechanically testing human DCM and HCM heart tissue and pig disease-model tissue.

Ju Chen

University of California-San Diego, CA·Physiology

Test whether mini-ALPK3, a shortened version of the ALPK3 kinase delivered by the muscle-targeting MyoAAV virus on the first day of life, prevents cardiomyopathy and early death in Alpk3 knockout mice.

The school

University of Washington: 81 labs on PI Pages, $1.7B a year on research, 694 research doctorates a year.

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