ArticleBiochemical pharmacology2022
CCR5 antagonist treatment inhibits vascular injury by regulating NADPH oxidase 1.
Article in Biochemical pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Citalopram Neuroendocrine Challenge Shows Altered Tryptophan and Kynurenine Metabolism in Migraine.Cells · 2022Trial
- The CX3CL1-CX3CR1 axis in HIV-associated inflammation and cardiometabolic disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- CCR5/CCL5-Dependent Mitochondrial Dysfunction Contributes to Angiotensin II-Induced Vascular Impairment in Mice.bioRxiv : the preprint server for biology · 2026Article
- PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis.Redox biology · 2026Article
- Targeting vascular inflammation and endothelial dysfunction with nanobodies: emerging therapeutic strategies for cardiovascular disease.Frontiers in immunology · 2026Review
- Three-Dimensional Perspectives on Inflammatory Regulation in Coronary Atherosclerosis: Integrated Mechanisms of Endothelial Priming, Lipid Metabolism, and Cytokine Synergy.Reviews in cardiovascular medicine · 2026Review
- Platelets induce endothelial cell mitochondrial dysfunction in myocardial infarction.Science advances · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Chemokine receptors in vascular biology: a review of current evidence, implications, and therapeutic targets for hypertension.Clinical science (London, England : 1979) · 2025Review
- Pharmacological advances in HIV treatment: from ART to long-acting injectable therapies.Archives of virology · 2025Review
- C-C chemokine ligand 5 from women subcutaneous adipose tissue has a central role in vascular aging.Cardiovascular diabetology · 2025Article
- The FKBPL-based therapeutic peptide, AD-01, protects the endothelium from hypoxia-induced damage by stabilising hypoxia inducible factor-α and inflammation.Journal of translational medicine · 2025Article
- Vascular Contractility Relies on Integrity of Progranulin Pathway: Insights Into Mitochondrial Function.Journal of the American Heart Association · 2025Article
- Connection Between HIV and Mitochondria in Cardiovascular Disease and Implications for Treatments.Circulation research · 2024Review
- In utero exposure to maternal diabetes exacerbates dietary sodium intake-induced endothelial dysfunction by activating cyclooxygenase 2-derived prostanoids.American journal of physiology. Endocrinology and metabolism · 2024Article
- Role of the CCL5 and Its Receptor, CCR5, in the Genesis of Aldosterone-Induced Hypertension, Vascular Dysfunction, and End-Organ Damage.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Adjusted vascular contractility relies on integrity of progranulin pathway: Insights into mitochondrial function.bioRxiv : the preprint server for biology · 2023Article
- Targeting CCL5 signaling attenuates neuroinflammation after seizure.CNS neuroscience & therapeutics · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChemokine (C- Cmotif) ligand 5 (CCL5) and its receptor C-C motif chemokine receptor 5 (CCR5), have been broadly studied in conjunction with infectious pathogens, however, their involvement in cardiovascular disease is not completely understood. NADPH oxidases (Noxs) are the major source of reactive oxygen species (ROS) in the vasculature. Whether the activation of Noxs is CCL5/CCR5 sensitive and whether such interaction initiates vascular injury is unknown. We investigated whether CCL5/CCR5 leads to vascular damage by activating Noxs. MATERIAL AND
methodsWe used rat aortic smooth muscle cells (RASMC) to investigate the molecular mechanisms by which CCL5 leads to vascular damage and carotid ligation (CL) to analyze the effects of blocking CCR5 on vascular injury.
resultsCCL5 induced Nox1 expression in concentration and time-dependent manners, with no changes in Nox2 or Nox4. Maraviroc pre-treatment (CCR5 antagonist, 40uM) blunted CCL5-induced Nox1 expression. Furthermore, CCL5 incubation led to ROS production and activation of Erk1/2 and NFkB, followed by increased vascular cell migration, proliferation, and inflammatory markers. Notably, Nox1 inhibition (GKT771, 10uM) blocked CCL5-dependent effects. In vivo, CL induced pathological vascular remodeling and inflammatory genes and increased Nox1 and CCR5 expression. Maraviroc treatment (25 mg/Kg/day) reduced pathological vascular growth and Nox1 expression.
conclusionsOur findings suggest that CCL5 activates Nox1 in the vasculature, leading to vascular injury likely via NFkB and Erk1/2. Herein, we place CCR5 antagonists and/or Nox1 inhibitors might be preeminent antiproliferative compounds to reduce the cardiovascular risk associated with medical procedures (e.g. angioplasty) and vascular diseases associated with vascular hyperproliferation.
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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.