Cameron Mccarthy
University of South Carolina-Columbia, SC·Physiology
Diabetes affects more than 463 million people worldwide and makes strokes both more likely and more damaging. When blood flow to the brain is cut off (ischemia), people with diabetes suffer greater brain injury and recover less well.
- Fields
Physiology
Neuroscience
Pharmacology
- Topics
diabetes
ischemic stroke
stroke recovery
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Test whether loss of OGT, the enzyme that adds O-GlcNAc sugar tags to proteins, protects parenchymal arterioles from dysfunction before stroke in mice made diabetic with a high-fat diet and low-dose streptozotocin.
- Determine whether reducing OGA, the enzyme that removes O-GlcNAc tags, worsens injury to brain cells and vessels after stroke induced by a clot in the middle cerebral artery of diabetic mice.
- Compare long-term functional recovery and behavior after stroke in diabetic mice with altered OGT or OGA levels, to test whether vessel O-GlcNAcylation impairs recovery.
- Model diabetic conditions in cultured brain microvascular endothelial and smooth muscle cells by exposing them to high glucose and the fatty acid palmitate, to study O-GlcNAc effects on vessel cells.
More about the research
Damage to blood vessels is the main cause of these outcomes. Still, it is not well understood why blood vessels in the diabetic brain are so vulnerable. That gap stands in the way of reducing illness and death from stroke in people with diabetes.
Why it matters
People with diabetes face higher stroke risk, worse brain damage and poorer recovery. If chronic O-GlcNAc tagging of proteins in brain blood vessels proves to be a cause, the enzymes OGT and OGA could become new therapeutic targets. Drugs aimed at them might help protect the brain's blood vessels in diabetes, lower stroke risk and improve recovery.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Gordon Meares
Ohio State University, OH·Neuroscience
Test whether deleting PERK, an ER stress sensor, in astrocytes or microglia improves outcome after experimental stroke, using mice with cell-specific PERK loss and middle cerebral artery occlusion.
Risheng Xu
Johns Hopkins University, MD·Neuroscience·Early-career
Identify which mast-cell inflammatory signals, such as TNFα and CCL2, are controlled by the receptor Mrgprb2 after ischemic stroke induced by transient middle cerebral artery occlusion in mice.
Jason D Huber
West Virginia University, WV·Pharmacology
Test whether NL-1, a compound that binds the mitochondrial protein mitoNEET, prevents ferroptosis (iron-dependent cell death) in a four-cell Transwell blood-brain barrier model after oxygen-glucose deprivation and reperfusion.
The school
University of South Carolina-Columbia: 22 labs on PI Pages, $277M a year on research, 425 research doctorates a year.
Reach out
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