Merline Benny
University of Miami, FL·Medicine & Clinical Research
Advances in newborn care now help many more preterm babies survive. As adults, though, they face higher risks of high blood pressure, ischemic heart disease and heart failure.
- Fields
Medicine & Clinical Research
Physiology
Microbiology & Immunology
- Topics
gasdermin D
pyroptosis
inflammation
- Grants
- 2 known grants, through Feb 2031
What they work on
- Test whether genetic deletion or drug inhibition of gasdermin D (GSDMD) protects newborn mice exposed to excess oxygen from vascular and cardiac dysfunction, measured in both newborn and adult mice.
- Assess vessel stiffness, remodeling, blood pressure, heart function and new vessel growth in GSDMD-deficient mice exposed to neonatal hyperoxia or room air, along with molecular studies.
- Define how GSDMD in endothelial cells, the cells lining blood vessels, drives hyperoxia-induced vascular inflammation, pyroptosis and remodeling, using mice that lack GSDMD only in these cells.
- Investigate whether pyroptotic endothelial cells signal to nearby smooth muscle cells and push them toward scarring, or profibrotic, responses through GSDMD.
More about the research
Preterm infants are often given extra oxygen, and even those who are not still face far more oxygen than in the womb. This excess oxygen, called hyperoxia, can inflame and damage the immature blood vessel system. Why this harm lasts into adulthood is unknown, and no therapy prevents it.
Why it matters
People born preterm face a lifelong higher risk of hypertension, ischemic heart disease and heart failure, and no therapy currently prevents it. If blocking gasdermin D reduces the vascular damage caused by excess oxygen in newborns, GSDMD could become a target for treatments that protect the heart and blood vessels of preterm survivors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yuanjun Shen
Binghamton University, NY·Medicine & Clinical Research·Early-career
Examine how Vps34, an enzyme that drives smooth muscle overgrowth, is activated in PAH lung arteries through Akt-dependent loss of phosphorylation at Ser164, including candidate phosphatases identified by computer analysis.
Chen Yuan Kam
University of California-Los Angeles, CA·Biology·Early-career
Track endothelial cell behaviors, such as migration within existing vessels, that prune and shape the skin vascular network in newborn mice, using longitudinal intravital imaging.
Mohammad Badran
University of Missouri-Columbia, MO·Physiology
Test whether the MR blockers spironolactone and finerenone reverse coronary microvascular dysfunction in obese male and female mice exposed to short- or long-term intermittent hypoxia, a mouse model of sleep apnea.
The school
University of Miami: 30 labs on PI Pages, $559M a year on research, 297 research doctorates a year.
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