ArticleJournal of the American Heart Association2025
RORγt Mediates Angiotensin II-Induced Pressor Responses, Microglia Activation, and Neuroinflammation by Disrupting the Blood-Brain Barrier in Rats.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- MFSD2A in health and disease: lysolipid transport, barrier physiology, and translational boundaries.Molecular biomedicine · 2026Review
- Neurovascular Unit Dysfunction and Neural Barrier Pathology in Dysautonomia: Molecular Links to Cardiovascular Autonomic Failure.International journal of molecular sciences · 2026Review
- The regulatory network of Mfsd2a in cerebral ischemia: a novel time-targeted intervention framework.Molecular biology reports · 2026Review
- SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice.Redox biology · 2026Article
- Central Sympathetic Nerve Activation-Mediated Hypertension: Target Mechanisms and Multimodal Interventions-From Basic Research to Clinical Translation.International journal of molecular sciences · 2026Review
- Role of Exercise in Modulating the Brain-Heart Axis in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Angiotensin III induces disruption of blood-brain barrier integrity in vitro in bEnd.3 brain endothelial cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Uncovering immune pathways for therapeutic targeting of hypertension.Expert opinion on therapeutic targets · 2025Review
- Hypertension Increases Susceptibility to Lead-Induced Microglial Polarization via ANT1-Mediated Mitochondrial DNA/cGAS/STING Signaling.Research (Washington, D.C.) · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundThe RORγt (nuclear receptor retinoid-related orphan receptor γt) has been identified as a master transcription factor critical for the differentiation of T helper 17 cells, the primary source of IL-17A (interleukin-17A). We previously demonstrated that IL-17A promotes neuroinflammation and sympathetic excitation, contributing to cardiac dysfunction in heart failure and angiotensin II (ANG II)-induced hypertension. The present study sought to determine whether inhibiting RORγt, thereby reducing IL-17A production, could attenuate microglial activation, neuroinflammation, and sympathetic excitation by preserving the integrity of the blood-brain barrier (BBB) in ANG II-induced hypertensive rats.
methodsRats underwent a 2-week subcutaneous infusion of ANG II, with concurrent daily subcutaneous administration of the RORγt inhibitor digoxin or vehicle.
resultsCompared with controls, ANG II-infused rats exhibited elevated IL-17A levels in both the periphery and brain, along with increased blood pressure and sympathetic tone-effects that were significantly attenuated by inhibiting RORγt with digoxin. ANG II-infused rats also displayed heightened BBB permeability, decreased expression of the BBB regulator Mfsd2a (major facilitator superfamily domain-containing protein 2a), increased caveolar transcytosis, and degradation of tight junction proteins in BBB endothelial cells within the hypothalamic paraventricular nucleus, a key autonomic regulatory brain center, all of which were alleviated by digoxin. Additionally, ANG II-infused rats showed marked microglial activation and elevated expression of proinflammatory cytokines within the paraventricular nucleus, both of which were mitigated by digoxin.
conclusionsThese findings suggest that RORγt inhibition reduces neuroinflammation and sympathetic activation to ameliorate ANG II-induced hypertension, likely by mitigating IL-17A-induced BBB disruption and microglial activation in the paraventricular nucleus.
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