Shah Ali
Columbia University, NY·Medicine & Clinical Research
After a heart attack, the damaged heart muscle is replaced by scar tissue, a process called cardiac fibrosis. Early on, this scar helps by keeping the weakened wall from tearing.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
cardiac fibrosis
myocardial infarction
heart attack
- Grants
- 1 known grant, through Mar 2028
What they work on
- Build a genetic mouse model in which the biotin-tagging enzyme TurboID sits in the endoplasmic reticulum of cardiac fibroblasts, so the proteins these scar-forming cells secrete can be labeled in living animals.
- Profile the proteins secreted by cardiac fibroblasts in the uninjured adult mouse heart with the TurboID model, creating a baseline for later comparisons.
- Compare the fibroblast secretome of newborn and adult mouse hearts at several times after myocardial infarction, focusing on extracellular matrix proteins, proteases and pro-fibrotic signaling ligands.
More about the research
Over time, though, it stiffens the heart and weakens its pumping, and there are no treatments for it. Fibrosis is also common in ischemic heart disease, diabetes and aging. Newborn mouse hearts behave differently. In the first few days of life they can regrow muscle after injury, and the scar that forms during this window disappears within about a month. How the newborn heart clears its scar is unknown. The project proposes that studying this process could point to anti-scarring therapies for the adult heart.
Why it matters
Many people who survive a heart attack, along with people with diabetes or aging hearts, develop stiff scar tissue in the heart muscle that impairs pumping, and no treatment targets it. Identifying the secreted proteins that let the newborn heart dissolve its scar could point to ways of reducing or resolving scar in adult hearts, which may help preserve heart function in these patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Bradford Hill
University of Louisville, KY·Physiology
Determine how alternative splicing of Pkm, which switches fibroblasts between the slower Pkm2 and faster Pkm1 enzyme forms, changes cardiac fibroblast metabolism and the amount of fibrosis after myocardial infarction.
Xiaolei Liu
Temple University, PA·Physiology
Determine the molecular pathways and targets through which lymphatic growth in the heart improves cardiomyocyte survival after myocardial infarction, building on survival signals such as Reelin released by lymphatic endothelial cells.
Joseph Hill
University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research
Determine how endothelial Fli1 protects the heart under ischemic stress, using tamoxifen-inducible mice that lack Fli1 only in blood vessel lining cells, and manipulate Fli1 activity in models of ischemic heart disease.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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