Key result
Knockout of immunoproteasome subunit β2i markedly reversed DOCA/salt-induced systolic blood pressure elevation, cardiac fibrosis, and inflammation in mice.
Why the study?
Does knockout of immunoproteasome subunit β2i ameliorate cardiac fibrosis and inflammation in DOCA/salt hypertensive mice?
Population
Wild-type and β2i knockout mice subjected to uninephrectomy and deoxycorticosterone-acetate/salt treatment
Comparison
Knockout of immunoproteasome subunit β2i vs Wild-type mice with DOCA/salt treatment and sham…
Design
Preclinical
Follow-up
21 days
Authors
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Identifies β2i inhibition as a potential therapeutic target for hypertensive heart disease; leaves open.
Does knockout of immunoproteasome subunit β2i ameliorate cardiac fibrosis and inflammation in DOCA/salt hypertensive mice?
Knockout of the immunoproteasome subunit β2i attenuates cardiac fibrosis and inflammation in a DOCA/salt hypertensive mouse model, suggesting a potential therapeutic target for hypertensive heart disease.
Bi et al. (2017) studied DOCA/salt-induced hypertension. β2i knockout vs. Wild-type mice was evaluated on Cardiac fibrosis, inflammation, and systolic blood pressure. Knockout of immunoproteasome subunit β2i markedly reversed DOCA/salt-induced systolic blood pressure elevation, cardiac fibrosis, and inflammation in mice.
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