Anita Saraf
University of Pittsburgh, PA·Medicine & Clinical Research·Early-career
Adults living with congenital heart disease (CHD), heart defects present from birth, are the fastest-growing group of adult heart patients worldwide. Many people with severe forms now survive into adulthood.
- Fields
Medicine & Clinical Research
Physiology
Genetics
- Topics
congenital heart disease
hypoplastic left heart syndrome
induced pluripotent stem cells
- Grants
- 1 known grant, through Feb 2027
What they work on
- Determine how inflammatory cytokines, which stay chronically elevated in single-ventricle patients, change calcium handling and contraction in iPSC-derived heart muscle cells carrying hypomorphic NOTCH1 mutations from HLHS patients.
- Determine how pressures like those in the body's circulation affect calcium handling and contractility in NOTCH1-deficient cardiomyocytes, to understand the causes of arrhythmia and heart failure.
- Engineer hypomorphic NOTCH1 mutations into control induced pluripotent stem cells with CRISPR gene editing, to compare with patient-derived cells and confirm the mutation's effects.
More about the research
However, they develop irregular heart rhythms (arrhythmias) and heart failure at high rates, and the cause is unknown. Studying these defects is hard because there are few useful animal models. This project instead uses heart muscle cells grown from patients' own stem cells to study one severe defect, hypoplastic left heart syndrome (HLHS), in which the left side of the heart is underdeveloped.
Why it matters
Adults with severe congenital heart disease, including survivors of hypoplastic left heart syndrome, often suffer arrhythmias and heart failure without a known cause. Finding out how NOTCH1 mutations, inflammation and pressure disrupt heart cell function could reveal new treatment targets. It could also help create better animal models of this disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Martin Morad
University of South Carolina-Columbia, SC·Physiology
Compare calcium-signaling defects caused by CPVT1 mutations in different regulatory regions of the cardiac calcium-release channel RyR2 in maturated human iPSC-derived heart cells, reverse them by editing the sequence back, and test drug responses.
Haodi Wu
University of Pittsburgh, PA·Genetics
Define how removing NIPBL changes heart-cell function and gene activity, using human iPSC-derived heart muscle cells with a dTAG degradation switch, functional assays and single-cell RNA sequencing.
Lei Yang
Indiana University-Purdue University-Indianapolis, IN·Biology
Determine how the human lncRNA MCRL1 and its partner protein β-Catenin switch on heart genes and switch off blood genes during mesoderm specification. The work uses MCRL1-knockout human embryonic stem cells differentiated toward heart cells.
The school
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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