Francesca Briganti
University of California-San Diego, CA·Medicine & Clinical Research·Early-career
Dilated cardiomyopathy (DCM) is a disease in which the heart muscle stretches and weakens, often leading to heart failure and early death. Harmful variants in more than 50 genes can cause it, but how they damage the heart is poorly understood, and no therapies target a patient's specific mutation.
- Fields
Medicine & Clinical Research
Genetics
Biomedical Engineering
- Topics
dilated cardiomyopathy
heart failure
microRNA
- Grants
- 1 known grant, through Jul 2027
What they work on
- 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.
- Identify target genes of candidate miRNAs that regulate the sarcomere and contraction, and test their effects in engineered heart tissues and a mouse model of DCM.
- Compare the target genes of miRNAs that help only specific DCM mutations with those that help all DCM lines, to test whether their target sets differ.
More about the research
This project asks whether some of the heart's own regulators could point to new treatments. MicroRNAs (miRNAs) are small RNA molecules that turn down the activity of other genes. Some of them rise in end-stage heart failure.
Why it matters
Patients with dilated cardiomyopathy currently have no mutation-specific treatments. By finding which miRNAs and target genes relieve contraction defects, and whether they act on all genetic forms of DCM or only some, this work could reveal new drug targets. It could also lay groundwork for personalized, mechanism-based therapies for people carrying DCM-causing mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xuebing Wu
Columbia University, NY·Genetics
Test whether RPL3L ribosomes, which replace the common ribosomal protein RPL3 in muscle, promote protein homeostasis in heart muscle cells, using human cell lines and mice expressing mainly RPL3 or RPL3L.
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.
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.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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