RCAN1-Mediated Calcineurin Impairment Drives Sympathetic Outflow in Hypertension
RCAN1-mediated calcineurin hypoactivity in the PVN augments sympathetic outflow by promoting synaptic expression and activity of α2δ-1-bound NMDARs in SHR. These findings identify a novel molecular mechanism underlying sympathetic overactivity in genetic hypertension and suggest potential therapeutic targets for neurogenic hypertension.
Authors
- Jian-Ying Shao
- Zengyou Ye (ORCID: https://orcid.org/0000-0003-1106-5371)
- Hui‐Lin Pan (ORCID: https://orcid.org/0000-0001-8444-3770)
- Jingjing Zhou (ORCID: https://orcid.org/0000-0001-5859-9827)
- Shao-Rui Chen (ORCID: https://orcid.org/0000-0002-0426-8202)
Institutions
- The University of Texas MD Anderson Cancer Center (US)
Publication Details
- Journal
- Circulation Research
- Published
- 2025-06-13
- DOI
- https://doi.org/10.1161/circresaha.124.325975
- Citations
- 3
- Primary Topic
- Signaling Pathways in Disease
- Type
- article
- Field-Weighted Citation Impact
- 2.42