Michal Laniado Schwartzman
New York Medical College, NY·Pharmacology
Obesity raises the risk of diabetes, high blood pressure, heart attack and stroke, but the molecular links between extra body fat and damage to the heart and blood vessels are still poorly understood. This research centers on one candidate link.
- Fields
Pharmacology
Physiology
Medicine & Clinical Research
- Topics
20-hydroxyeicosatetraenoic acid
G-protein coupled receptor
obesity
- Grants
- 1 known grant, through Feb 2027
What they work on
- Test whether removing Gpr75 only from endothelial cells, the cells lining blood vessels, protects mice from diet-driven obesity, high blood sugar, insulin resistance and hypertension.
- Determine whether deleting Gpr75 specifically in fat cells (adipocytes) prevents the 20-HETE-driven fat-cell enlargement, impaired insulin signaling and mitochondrial dysfunction seen in diet-induced obesity in mice.
- Examine how 20-HETE binding to GPR75 drives communication between adipocytes and endothelial cells that worsens cardiovascular and metabolic complications of obesity.
- Define the endothelial pathways engaged by 20-HETE-GPR75 signaling, including disruption of eNOS (the enzyme that makes the vessel-relaxing gas nitric oxide), induction of ACE, and activation of NF-κB inflammation.
More about the research
It is a receptor on the cell surface called GPR75, a G-protein coupled receptor, which is a type of sensor that relays outside signals into the cell. The lipid that binds it is 20-HETE (20-hydroxyeicosatetraenoic acid), a fat-derived signaling molecule that constricts blood vessels and promotes inflammation.
Why it matters
Obesity is a worldwide epidemic and a risk factor for diabetes, cardiovascular disease, liver disease and severe infections such as COVID-19. Human genetic data link loss of GPR75 function to protection from obesity. Clarifying how GPR75 activation by 20-HETE worsens fat gain, insulin resistance and blood-vessel dysfunction could point to new drug targets for treating obesity and its heart and metabolic complications.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kafait U Malik
University of Tennessee Health Science Center, TN·Pharmacology
Determine how the brain's arachidonic acid/ALOX15 pathway in the paraventricular nucleus contributes to angiotensin II-induced hypertension in female and male mice, using adenovirus gene tools and radiotelemetry.
Naomi Hamburg
Boston University, MA·Medicine & Clinical Research
Test whether type 2 diabetes and related cardiometabolic traits are linked to organelle stress (mitochondrial dysfunction and ER stress) in fresh endothelial cells from 450 Framingham Heart Study participants.
Pooneh Bagher
University of Nebraska Medical Center, NE·Physiology
Determine whether hemoglobin alpha in artery-lining endothelial cells becomes glycated in a mouse model of diabetes, including at sites within its putative eNOS-binding domain.
The school
New York Medical College: 3 labs on PI Pages, $22M a year on research, 12 research doctorates a year.
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