ReviewInternational journal of molecular sciences2021
Toll-Like Receptors in the Pathogenesis of Essential Hypertension. A Forthcoming Immune-Driven Theory in Full Effect.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The role of vascular aging, bone marrow and immune system in hypertension.Cell death discovery · 2026Review
- Editorial: Endothelium, innate immunity and coagulation in hematological disorders.Frontiers in medicine · 2026Article
- Targeting vascular inflammation and endothelial dysfunction with nanobodies: emerging therapeutic strategies for cardiovascular disease.Frontiers in immunology · 2026Review
- Diagnostic Utility of Combining Homocysteine, Lipoprotein-Associated Phospholipase A2, and the C-Reactive Protein-to-Albumin Ratio for Assessing Carotid Atherosclerosis and Plaque Stability in Patients with Essential Hypertension.Cardiovascular toxicology · 2025Article
- Genetics and Epigenetics in Acquired Hemophilia A: From Bench to Bedside.Current issues in molecular biology · 2024Review
- Toll-like receptors in health and disease.MedComm · 2024Review
- Article
- Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022Review
- Pathogenetic Mechanisms of Hypertension-Brain-Induced Complications: Focus on Molecular Mediators.International journal of molecular sciences · 2022Review
- Pathogenesis of (smoking-related) non-communicable diseases-Evidence for a common underlying pathophysiological pattern.Frontiers in physiology · 2022Review
- Osthole Regulates Secretion of Pro-Inflammatory Cytokines and Expression ofJournal of inflammation research · 2022Article
- Molecular Advances in Hypertension and Blood.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Essential hypertension (EH) is a highly heterogenous disease with a complex etiology. Recent evidence highlights the significant contribution of subclinical inflammation, triggered and sustained by excessive innate immune system activation in the pathogenesis of the disease. Toll-like receptors (TLRs) have been implied as novel effectors in this inflammatory environment since they can significantly stimulate the production of pro-inflammatory cytokines, the migration and proliferation of smooth muscle cells and the generation of reactive oxygen species (ROS), facilitating a low-intensity inflammatory background that is evident from the very early stages of hypertension. Furthermore, the net result of their activation is oxidative stress, endothelial dysfunction, vascular remodeling, and finally, vascular target organ damage, which forms the pathogenetic basis of EH. Importantly, evidence of augmented TLR expression and activation in hypertension has been documented not only in immune but also in several non-immune cells located in the central nervous system, the kidneys, and the vasculature which form the pathogenetic core systems operating in hypertensive disease. In this review, we will try to highlight the contribution of innate immunity in the pathogenesis of hypertension by clarifying the deleterious role of TLR signaling in promoting inflammation and facilitating hypertensive vascular damage.
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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.