David L. Mattson
Augusta University, GA·Physiology
High blood pressure (hypertension) is the single largest contributor to death and disease worldwide. In 30–50% of people with hypertension, blood pressure rises with salt intake.
- Fields
Physiology
Microbiology & Immunology
Medicine & Clinical Research
- Topics
hypertension
blood pressure
Dahl salt-sensitive rat
- Grants
- 2 known grants, through Jun 2027
What they work on
- Determine how animal-based versus grain-based dietary protein changes gut microbial metabolites such as carnitine and propionate, and whether these metabolites alter NOX2 in T cells and salt-sensitive hypertension in Dahl SS rats.
- Test whether NOX2 (a free radical-producing enzyme) in kidney-infiltrating CD4+ T cells raises renal vascular resistance and drives hypertension, by transferring wild-type or NOX2-deficient T cells into T cell-lacking SS rats.
- Test whether CD14 protects against salt-sensitive hypertension and kidney damage by inhibiting TLR4 signaling in kidney macrophages, using genetically engineered Dahl SS rats lacking CD14.
- Determine whether NOX2 in macrophages raises blood pressure in high-salt-fed SS rats, an effect that CD14 may dampen in females and TLR4 may amplify in males.
- Test whether TLR4 and CD14 alter pressure natriuresis-diuresis (salt and water excretion in response to blood pressure) and blood flow within the kidney through NOX2-derived free radicals, measured in conscious rats.
More about the research
These salt-sensitive patients die at higher rates and suffer more kidney damage. Immune cells and inflammation are known to play a part, but what switches the immune system on in hypertension is unclear. Both projects use the Dahl salt-sensitive (SS) rat, a rat strain that mimics the human condition. They study how immune cells in the kidney release free radicals, reactive molecules that cause damage, through the enzyme NOX2. This process drives up blood pressure and harms the kidney.
Why it matters
Salt-sensitive hypertension affects a large share of people with high blood pressure and carries extra risk of kidney damage and death. Identifying immune pathways such as T-cell NOX2 and macrophage CD14 could point to new treatment targets. Showing how dietary protein source shapes these pathways through gut microbes could inform dietary advice. The sex differences found in CD14 effects may also help explain why risk differs between women and men.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Nicholas Ferreri
New York Medical College, NY·Physiology
Determine which kidney tubule cells produce the TNF that limits salt-driven blood pressure rises, using mice lacking TNF in the thick ascending limb or distal nephron plus cell-specific TNF-silencing lentiviruses.
Thomas Kleyman
University of Pittsburgh, PA·Physiology
Test whether the delta subunit of the epithelial sodium channel in immune cells drives salt-sensitive hypertension, by transferring dendritic cells and monocytes derived from human induced pluripotent stem cells carrying SCNN1D deletions or mutations into immune-deficient mice.
Clintoria Williams
Wright State University, OH·Physiology
Test whether zinc supplementation in early CKD restores zinc balance, limits kidney sodium reabsorption, lowers blood pressure and slows disease in calcineurin inhibitor-treated mice and Akita diabetic kidney disease mice.
The school
Augusta University: 11 labs on PI Pages, $166M a year on research, 37 research doctorates a year.
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