Key result
T-cell NADPH oxidase 2 amplifies salt-sensitive hypertension and renal damage in a rat model.
Why the study?
Does the adoptive transfer of T cells lacking functional NADPH oxidase 2 reduce salt-sensitive hypertension and renal damage in T cell-deficient Dahl SS rats?
Does the adoptive transfer of T cells lacking functional NADPH oxidase 2 reduce salt-sensitive hypertension and renal damage in T cell-deficient Dahl SS rats?
Reactive oxygen species from NADPH oxidase 2 in T cells exacerbate salt-sensitive hypertension and renal damage in a rat model.
Findings in Dahl rats should not alter management; leaves open T-cell NOX2 targeting in human salt-sensitive hypertension.
Our current work used the adoptive transfer of T cells that lack functional NADPH oxidase 2 into a genetically T cell-deficient Dahl salt-sensitive (SS) rat model. The results demonstrated that reactive oxygen species produced by NADPH oxidase 2 in T cells participate in the amplification of SS hypertension and associated renal damage and identifies a potential mechanism that exacerbates the salt-sensitive phenotype.
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Walton et al. (2023) studied Salt-sensitive hypertension and associated renal damage. Adoptive transfer of T cells lacking functional NADPH oxidase 2 was evaluated on Amplification of SS hypertension and associated renal damage. Reactive oxygen species produced by NADPH oxidase 2 in T cells participate in the amplification of salt-sensitive hypertension and associated renal damage in a Dahl rat model.
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