Translational research : the journal of laboratory and clinical medicine · 2026
STIM1 deletion in regulatory T cells restores redox balance and protects against hypertension-induced cardiovascular complications.
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Srinivas B, Alluri K, Fortuno P, Matrougui K
Аннотация
BACKGROUND: Regulatory T cells (Tregs) play a protective role in cardiovascular diseases, but the redox-regulated mechanisms governing their survival remain unclear. Stromal interaction molecule 1 (STIM1), a key calcium sensor, is implicated in oxidative stress and T cell apoptosis. This study investigates how Treg-specific deletion of STIM1 modulates redox signaling and mitigates renovascular hypertension and associated cardiovascular complications.
METHODS: STIM1 was selectively deleted in Tregs using a Cre-loxP approach. Mice were subjected to 2-kidney-1-clip (2K1C) surgery to induce renovascular hypertension. Endpoints included blood pressure, cardiac and pulmonary pathology, endothelial function, redox markers (ROS, SOD, BH4), nitric oxide bioavailability, and inflammatory cytokines.
RESULTS: STIM1 deletion in Tregs prevented in vitro angiotensin II-induced Treg cell death and protected against in vivo hypertension, cardiac hypertrophy, endothelial dysfunction, and fibrosis. Interestingly, STIM1-deficient Tregs preserved eNOS phosphorylation and nitrate levels, reduced ROS, and restored SOD and BH4 levels. Inflammatory cytokines and TGF-β1 were also significantly attenuated in knockout mice.
CONCLUSIONS: STIM1 in Tregs is a significant mechanism of immune survival and redox homeostasis in renovascular hypertension. Its deletion alleviates oxidative stress, vascular injury, and fibrosis, highlighting a promising immuno-redox target for cardiovascular disease intervention.
METHODS: STIM1 was selectively deleted in Tregs using a Cre-loxP approach. Mice were subjected to 2-kidney-1-clip (2K1C) surgery to induce renovascular hypertension. Endpoints included blood pressure, cardiac and pulmonary pathology, endothelial function, redox markers (ROS, SOD, BH4), nitric oxide bioavailability, and inflammatory cytokines.
RESULTS: STIM1 deletion in Tregs prevented in vitro angiotensin II-induced Treg cell death and protected against in vivo hypertension, cardiac hypertrophy, endothelial dysfunction, and fibrosis. Interestingly, STIM1-deficient Tregs preserved eNOS phosphorylation and nitrate levels, reduced ROS, and restored SOD and BH4 levels. Inflammatory cytokines and TGF-β1 were also significantly attenuated in knockout mice.
CONCLUSIONS: STIM1 in Tregs is a significant mechanism of immune survival and redox homeostasis in renovascular hypertension. Its deletion alleviates oxidative stress, vascular injury, and fibrosis, highlighting a promising immuno-redox target for cardiovascular disease intervention.