ArticleAmerican journal of physiology. Heart and circulatory physiology2019
Angiotensin II-induced hypertension and cardiac hypertrophy are differentially mediated by TLR3- and TLR4-dependent pathways.
Article in American journal of physiology. Heart and circulatory physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
- Sex differences in TLR4 expression in SHR do not contribute to sex differences in blood pressure or the renal T cell profile.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Trial
- Gut Dysbiosis Promotes Myocardial Hypertrophy via GBP2b/GBP1 in Chronic Colitis.Circulation research · 2026Article
- Metabolic-inflammatory memory: the common pathological basis and therapeutic targets of metabolic syndrome.Reviews in endocrine & metabolic disorders · 2026Review
- LARP1 acts as a key mediator in preventing angiotensin II-induced cardiac dysfunction and fibrosis.Cell & bioscience · 2025Article
- Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025Review
- Toll-like Receptors 1, 3 and 7 Activate Distinct Genetic Features of NF-κB Signaling and γ-Protocadherin Expression in Human Cardiac Fibroblasts.Inflammation · 2025Article
- Therapeutic potential of Withaferin A in cancer-induced muscle and cardiac wasting.Journal of ovarian research · 2025Review
- Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II-Induced Cardiac Hypertrophy.Journal of cellular and molecular medicine · 2025Article
- Article
- Study on the Regulated Cell Death of Hypertrophic H9c2 Cells Induced by Au:Ag Nanoparticles.International journal of nanomedicine · 2025Article
- Jaranol: a compound with therapeutic activity against pathological cardiac remodelling via multi-target inhibition of the Snai3/TLR2 and NF-κB signaling pathways.Frontiers in pharmacology · 2025Article
- The Role of Sterile Inflammation in Thrombosis: Consequences for Cardiovascular Disease and COVID-19.Mediators of inflammation · 2025Review
- The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
- Cardiomyocyte-specific deletion of TLR4 attenuates angiotensin II-induced hypertension and cardiac remodeling.Frontiers in cardiovascular medicine · 2023Article
- Review
- Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022Review
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLR) are key components of the innate immune system that elicit inflammatory responses through the adaptor proteins myeloid differentiation protein 88 (MyD88) and Toll-interleukin receptor domain-containing adaptor protein-inducing interferon-β (TRIF). Previously, we demonstrated that TRIF mediates the signaling of angiotensin II (ANG II)- induced hypertension and cardiac hypertrophy. Since TRIF is activated selectively by TLR3 and TLR4, our goals in this study were to determine the roles of TLR3 and TLR4 in mediating ANG II-induced hypertension and cardiac hypertrophy, and associated changes in proinflammatory gene expression in heart and kidney. In wild-type (WT) mice, ANG II infusion (1,000 ng·kg
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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.