Yuanjun Shen
Binghamton University, NY·Medicine & Clinical Research·Early-career
Pulmonary arterial hypertension (PAH) is a progressive, rapidly fatal disease with no cure. In PAH, the small arteries of the lungs thicken and narrow, which raises blood pressure in the lungs.
- Fields
Medicine & Clinical Research
Physiology
Pharmacology
- Topics
pulmonary arterial hypertension
pulmonary hypertension
vascular remodeling
- Grants
- 1 known grant, through Apr 2028
What they work on
- 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.
- Determine how Vps34 controls proliferation and survival of human PAH pulmonary artery smooth muscle cells through Vps15 and the TSC2–mTORC1 growth pathway, using siRNA silencing and drug inhibitors.
- Test whether molecular or drug-based inhibition of Vps34 reduces or reverses lung artery remodeling and right-heart enlargement in rodent models, including mice with SU5416/hypoxia-induced pulmonary hypertension.
More about the research
The right side of the heart then strains to pump blood, which eventually leads to heart failure. A key driver of this narrowing is that smooth muscle cells in the artery walls grow too much and resist dying. This project asks what switches on that overgrowth. It focuses on Vps34, an enzyme that the principal investigator found is overactive in these cells in PAH.
Why it matters
Patients with pulmonary arterial hypertension have no cure, and many die of right-heart failure. If blocking Vps34 proves able to stop smooth muscle overgrowth and reverse artery narrowing, this enzyme could become a new drug target. Such a drug might slow or reverse lung vessel remodeling in people with this disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jason Hong
University of California-Los Angeles, CA·Medicine & Clinical Research·Early-career
Define how asporin blocks both TGF-β and EGFR signaling and what controls its protein levels in PAH pulmonary artery smooth muscle cells, using receptor-binding, drug-synergy, protein-stability and ubiquitination assays.
Sanda Predescu
Rush University, IL·Medicine & Clinical Research
Validate that Xist, a long non-coding RNA that silences one X chromosome in females, is more highly expressed and active in female pulmonary arterial hypertension lung tissue and pulmonary artery endothelial cells.
Sasha Prisco
University of Minnesota, MN·Medicine & Clinical Research·Early-career
Determine whether Lactobacillus supplementation reduces harmful microtubule remodeling and improves right ventricular function in monocrotaline and Sugen-hypoxia rodent models of pulmonary arterial hypertension.
The school
Binghamton University: 14 labs on PI Pages, $161M a year on research, 132 research doctorates a year.
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