ArticleFrontiers in pharmacology2019
The Involvement of Renin-Angiotensin System in Lipopolysaccharide-Induced Behavioral Changes, Neuroinflammation, and Disturbed Insulin Signaling.
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Calcitriol and candesartan mitigate monosodium glutamate-exacerbated metabolic syndrome and MASLD/MASH in rats: modulation of GLuR5/Ketohexokinase/FoxO1 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Microglial activation and RAS signaling: a dual-edged sword in neuroinflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- Biochemical, histopathological, and immunohistochemical study on the ameliorative effect of crocin against lipopolysaccharide‑induced hippocampal toxicity in male albino rats.BMC pharmacology & toxicology · 2025Article
- Effect of electroacupuncture on hypertensive and sympathetic excitability mechanism mediated by the paraventricular nucleus of the hypothalamus in spontaneous hypertensive rats.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Local patterns of genetic sharing between neuropsychiatric and insulin resistance-related conditions.Translational psychiatry · 2025Article
- Targeting Toll-like Receptor 4/Nuclear Factor-κB and Nrf2/Heme Oxygenase-1 Crosstalk via Trimetazidine Alleviates Lipopolysaccharide-Induced Depressive-like Behaviors in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Stress responses to bacterial and viral mimetics in polycystic ovary syndrome model rats.Brain, behavior, & immunity - health · 2024Article
- The Counteracting Effects of Ang II and Ang-(1-7) on the Function andGrowth of Insulin-secreting NIT-1 Cells.Current diabetes reviews · 2024Article
- Insulin in the regulation of the renin-angiotensin system: a new perspective on the mechanism of insulin resistance and diabetic complications.Frontiers in endocrinology · 2024Article
- Targeting the Renin-Angiotensin System (RAS) for Neuropsychiatric Disorders.Current neuropharmacology · 2024Article
- Antidepressant-like Effects of Renin Inhibitor Aliskiren in an Inflammatory Mouse Model of Depression.Brain sciences · 2022Article
- Cardiovascular therapeutics: A new potential for anxiety treatment?Medicinal research reviews · 2022Review
- Angiotensin II related glial cell activation and necroptosis of retinal ganglion cells after systemic hypotension in glaucoma.Cell death & disease · 2022Article
- Review
- Molecular mechanisms linking stress and insulin resistance.EXCLI journal · 2022Review
- Renin-angiotensin system: The underlying mechanisms and promising therapeutical target for depression and anxiety.Frontiers in immunology · 2022Review
- Article
- RNA-seq co-expression network analysis reveals anxiolytic behavior of mice with Efnb2 knockout in parvalbumin+ neurons.Molecular brain · 2021Article
- Neuroinflammation: A Signature or a Cause of Epilepsy?International journal of molecular sciences · 2021Review
- Insights into the actions of angiotensin-1 receptor (AT1R) inverse agonists: Perspectives and implications in COVID-19 treatment.EXCLI journal · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain insulin signaling is accounted for the development of a variety of neuropsychiatric disorders, such as anxiety and depression, whereas both inflammation and the activated renin-angiotensin system (RAS) are two major contributors to insulin resistance. Intriguingly, inflammation and RAS can activate each other, forming a positive feedback loop that would result in exacerbated unwanted tissue damage. To further examine the interrelationship among insulin signaling, neuroinflammation and RAS in the brain, the effect of repeated lipopolysaccharide (LPS) exposure and co-treatment with the angiotensin II (Ang II) receptor type 1 (AT1) blocker, candesartan (Cand), on anxiety and depression-like behaviors, RAS, neuroinflammation and insulin signaling was explored. Our results demonstrated that prolonged LPS challenge successfully induced the rats into anxiety and depression-like state, accompanied with significant neural apoptosis and neuroinflammation. LPS also activated RAS as evidenced by the enhanced angiotensin converting enzyme (ACE) expression, Ang II generation and AT1 expression. However, blocking the activated RAS with Cand co-treatment conferred neurobehavioral protective properties. The AT1 blocker markedly ameliorated the microglial activation, the enhanced gene expression of the proinflammatory cytokines and the overactivated NF-κB signaling. In addition, Cand also mitigated the LPS-induced disturbance of insulin signaling with the normalized phosphorylation of serine 307 and tyrosine 896 of insulin receptor substrate-1 (IRS-1). Collectively, the present study, for the first time, provided the direct evidence indicating that the inflammatory condition may interact with RAS to impede brain insulin pathway, resulting in neurobehavioral damage, and inhibiting RAS seems to be a promising strategy to block the cross-talk and cut off the vicious cycle between RAS and immune system.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.