NLRP3 Inflammasome Mediates Aldosterone-Induced Vascular Damage
Authors' conclusion
Together, these data demonstrate that NLRP3 inflammasome, through activation of IL-1R, is critically involved in the deleterious vascular effects of aldosterone
Study context
- Population
- Mice treated with vehicle or aldosterone (600 µg·kg-1·d-1 for 14 days by osmotic mini-pump) with 1% saline to drink; human PBMCs and hypertensive patients
- Comparison
- Aldosterone vs vehicle in wild-type (WT) and NLRP3-/-, Casp-1-/-, IL-1R-/- mice
- Outcome
- Vascular function and inflammatory profile
- Follow-up
- 14 days
Main finding
As reported in the abstract
- Long-term aldosterone infusion raised plasma IL-1β and caused vascular abnormalities
- Mice lacking IL-1R, NLRP3 or caspase-1 were protected from aldosterone-induced vascular damage
- In vitro, aldosterone stimulated NLRP3-dependent IL-1β secretion by bone marrow-derived macrophages via NF-κB signalling and ROS generation
- Chimeric mice with NLRP3-deficient hematopoietic cells: NLRP3 in immune cells mediates aldosterone-induced vascular damage
Further findings
Human PBMCs
- Aldosterone increased expression of NLRP3, active caspase-1 and mature IL-1β
NLRP3 inflammasome activity in hypertensive patients
- Hypertensive patients with hyperaldosteronism or normal aldosterone had increased NLRP3 inflammasome activity, suggesting the effect may be mediated through high BP
Original publication
NLRP3 Inflammasome Mediates Aldosterone-Induced Vascular Damage. Circulation. Published 1 November 2016. doi:10.
Summarised from the published abstract; every number is checked against it