ReviewJournal of molecular and cellular cardiology2011
Therapeutic targeting of innate immunity in the failing heart.
Review in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 45 citations in OpenAlex.
- QT Prolongation and Arrhythmias in Cancer Therapy: A Narrative Review of Mechanistic and Clinical Studies.Cardiovascular toxicology · 2026Review
- Heme catabolism and heme oxygenase-1-expressing myeloid cells in pathophysiology.Frontiers in immunology · 2024Review
- Off-Target Effects of Cancer Therapy on Development of Therapy-Induced Arrhythmia: A Review.Cardiology · 2023Review
- The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.ESC heart failure · 2021Article
- Melatonin as a protective agent in cardiac ischemia-reperfusion injury: Vision/Illusion?European journal of pharmacology · 2020Review
- Association of soluble interleukin-2 receptor α and tumour necrosis factor receptor 1 with heart failure: The Multi-Ethnic Study of Atherosclerosis.ESC heart failure · 2020Article
- Uncovering the Molecular Mechanism of the Qiang-Xin 1 Formula on Sepsis-Induced Cardiac Dysfunction Based on Systems Pharmacology.Oxidative medicine and cellular longevity · 2020Article
- The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure.Mediators of inflammation · 2018Review
- BEX1 is an RNA-dependent mediator of cardiomyopathy.Nature communications · 2017Article
- T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure.Scientific reports · 2017Article
- Pediatric and adult dilated cardiomyopathy represent distinct pathological entities.JCI insight · 2017Article
- Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.Scientific reports · 2017Article
- Non-coding RNAs in cardiac hypertrophy.The Journal of physiology · 2017Review
- A novel 72-kDa leukocyte-derived osteoglycin enhances the activation of toll-like receptor 4 and exacerbates cardiac inflammation during viral myocarditis.Cellular and molecular life sciences : CMLS · 2017Article
- Skeletal muscle inflammation and atrophy in heart failure.Heart failure reviews · 2017Review
- Expression of Adiponectin Receptors on Peripheral Blood Leukocytes of Hypertensive Children Is Associated with the Severity of Hypertension.BioMed research international · 2015Article
- Innate immune receptors in heart failure: Side effect or potential therapeutic target?World journal of cardiology · 2014Review
- Toll-like receptors 2 and 4 modulate autonomic control of heart rate and energy metabolism.Brain, behavior, and immunity · 2014Article
- Cardiopulmonary exercise capacity and preoperative markers of inflammation.Mediators of inflammation · 2014Article
- Toll-interacting protein (Tollip) negatively regulates pressure overload-induced ventricular hypertrophy in mice.Cardiovascular research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies suggest that the heart possesses an intrinsic system that is intended to delimit tissue injury, as well as orchestrate homoeostatic responses within the heart. The extant literature suggests that this intrinsic stress response is mediated, at least in part, by a family of pattern recognition receptors that belong to the innate immune system, including CD14, the soluble pattern recognition receptor for lipopolysaccharide, and Toll-like receptors 2, 3, 4, 5, 6, 7, and 9. Although this intrinsic stress response system provides a short-term adaptive response to tissue injury, the beneficial effects of this phylogenetically ancient system may be lost if myocardial expression of these molecules either becomes sustained and/or excessive, in which case the salutary effects of activation of these pathways are contravened by the known deleterious effects of inflammatory signaling. Herein we present new information with regard to activation of innate immune gene expression in the failing human heart, as well as review the novel TLR antagonists that are being developed for other indications outside of heart failure. This review will discuss the interesting possibility that the TLR pathway may represent a new target for the development of novel heart failure therapeutics. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."
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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.