Roberto Machado
University of Maryland, Baltimore, MD·Medicine & Clinical Research
Blood vessels in the lungs can be damaged in ways that become life-threatening. Their inner lining, the endothelium, is injured by inflammation and low oxygen, and vessel walls can be gradually rebuilt, or remodeled, until blood no longer flows normally.
- Fields
Medicine & Clinical Research
Physiology
Genetics
- Topics
pulmonary arterial hypertension
pulmonary hypertension
NAD signaling
- Grants
- 2 known grants, through Jun 2027
What they work on
- Define how NAMPT, the enzyme that makes the metabolic signaling molecule NAD, controls metabolic reprogramming in pulmonary artery endothelial cells during the pulmonary hypertension response.
- Determine how NAMPT regulates mitochondrial dynamics, the division and fusion of the cell's energy-producing structures, in pulmonary artery endothelial cells.
- Discover and validate NAMPT-centered biochemical and genetic biomarkers that predict susceptibility to pulmonary arterial hypertension and its prognosis.
- Test T-cell receptor repertoire profiling, a survey of the receptors carried by a patient's T cells, as a modifier and biomarker of acute chest syndrome risk in sickle cell disease.
- Interrogate RASA3, a signaling protein, and endothelial cell lipid droplets as molecular and therapeutic targets in mouse models of acute chest syndrome.
More about the research
Two projects study this lung vascular injury in different diseases: pulmonary arterial hypertension, a fatal and incurable form of high blood pressure in the lung arteries, and acute chest syndrome, a dangerous lung injury in people with sickle cell disease. Both pair mechanistic work in cells and mice with searches for genetic and biochemical biomarkers, measurable signals that predict who will get sick or how badly.
Why it matters
Pulmonary arterial hypertension has no cure and high mortality, and acute chest syndrome is a leading cause of death for people with sickle cell disease, a serious health disparity. Identifying NAMPT-linked pathways, RASA3 and endothelial lipid droplets as targets could point toward vessel-specific treatments, while blood and genetic biomarkers could help clinicians flag patients at higher risk and predict outcomes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Solomon Ofori-Acquah
Emory University, GA·Medicine & Clinical Research
Measure blood levels of HO-1, the heme-breaking enzyme, in sickle cell patients and transgenic mice, and test whether miR-494 and DNA methylation of the HMOX1 gene control it, by raising and lowering miR-494 in human blood immune cells.
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.
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.
The school
University of Maryland, Baltimore: 23 labs on PI Pages, $1.5B a year on research, 79 research doctorates a year.
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