ReviewCellular and molecular neurobiology2012
Angiotensin II AT(1) receptor blockers ameliorate inflammatory stress: a beneficial effect for the treatment of brain disorders.
Review in Cellular and molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 90 citations in OpenAlex.
- Mechanisms of angiotensin II to induce depression in diabetes.Diabetology international · 2025Review
- Higher Neuronal Facilitation and Potentiation with APOE4 Suppressed by Angiotensin II.Molecular neurobiology · 2024Article
- Angiotensin Receptor Blockers and Cognition: a Scoping Review.Current hypertension reports · 2024Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Higher Neuronal Facilitation and Potentiation with APOE4 Suppressed by Angiotensin II.Research square · 2023Article
- AT 1 inhibition mediated neuroprotection after experimental traumatic brain injury is dependent on neutrophils in male mice.Scientific reports · 2023Article
- Brain Renin-Angiotensin System: From Physiology to Pathology in Neuronal Complications Induced by SARS-CoV-2.Analytical cellular pathology (Amsterdam) · 2023Review
- Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases.Biomolecules · 2022Review
- AT2 activation does not influence brain damage in the early phase after experimental traumatic brain injury in male mice.Scientific reports · 2022Article
- Nanotechnology-Abetted Astaxanthin Formulations in Multimodel Therapeutic and Biomedical Applications.Journal of medicinal chemistry · 2022Review
- The AT1 Receptor Blocker Telmisartan Reduces Intestinal Mucus Thickness in Obese Mice.Frontiers in pharmacology · 2022Article
- Molecular mechanisms linking stress and insulin resistance.EXCLI journal · 2022Review
- Effect of prorenin peptide vaccine on the early phase of diabetic retinopathy in a murine model of type 2 diabetes.PloS one · 2022Article
- Telmisartan Inhibits the NLRP3 Inflammasome by Activating the PI3K Pathway in Neural Stem Cells Injured by Oxygen-Glucose Deprivation.Molecular neurobiology · 2021Article
- Transcriptomic Analysis of Mouse Brain After Traumatic Brain Injury Reveals That the Angiotensin Receptor Blocker Candesartan Acts Through Novel Pathways.Frontiers in neuroscience · 2021Article
- The Renin-Angiotensin System Modulates Dopaminergic Neurotransmission: A New Player on the Scene.Frontiers in synaptic neuroscience · 2021Review
- Systemic Candesartan Treatment Modulates Behavior, Synaptic Protein Levels, and Neuroinflammation in Female Mice That Express HumanFrontiers in neuroscience · 2021Article
- Candesartan Neuroprotection in Rat Primary Neurons Negatively Correlates with Aging and Senescence: a Transcriptomic Analysis.Molecular neurobiology · 2020Article
- The Effect of Pentoxifylline on Passive Avoidance Learning and Expression of Tumor Necrosis Factor-Alpha and Caspase-3 in the Rat Hippocampus Following Lipopolysaccharide-Induced Inflammation.Advanced biomedical research · 2019Article
- Candesartan ameliorates brain inflammation associated with Alzheimer's disease.CNS neuroscience & therapeutics · 2018Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 2 countries.
Funding
Abstract
Excessive allostatic load as a consequence of deregulated brain inflammation participates in the development and progression of multiple brain diseases, including but not limited to mood and neurodegenerative disorders. Inhibition of the peripheral and brain Renin-Angiotensin System by systemic administration of Angiotensin II AT(1) receptor blockers (ARBs) ameliorates inflammatory stress associated with hypertension, cold-restraint, and bacterial endotoxin administration. The mechanisms involved include: (a) decreased inflammatory factor production in peripheral organs and their release to the circulation; (b) reduced progression of peripherally induced inflammatory cascades in the cerebral vasculature and brain parenchyma; and (c) direct anti-inflammatory effects in cerebrovascular endothelial cells, microglia, and neurons. In addition, ARBs reduce bacterial endotoxin-induced anxiety and depression. Further pre-clinical experiments reveal that ARBs reduce brain inflammation, protect cognition in rodent models of Alzheimer's disease, and diminish brain inflammation associated with genetic hypertension, ischemia, and stroke. The anti-inflammatory effects of ARBs have also been reported in circulating human monocytes. Clinical studies demonstrate that ARBs improve mood, significantly reduce cognitive decline after stroke, and ameliorate the progression of Alzheimer's disease. ARBs are well-tolerated and extensively used to treat cardiovascular and metabolic disorders such as hypertension and diabetes, where inflammation is an integral pathogenic mechanism. We propose that including ARBs in a novel integrated approach for the treatment of brain disorders such as depression and Alzheimer's disease may be of immediate translational relevance.
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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.