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Cited by 344

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Toll-Like Receptor 4 Mediates Maladaptive Left Ventricular Remodeling and Impairs Cardiac Function After Myocardial Infarction

Open access
Timmers, Leo, Sluijter, Joost P.G., van Keulen, J. Karlijn, Hoefer, Imo E., Nederhoff, Marcel G.J., Goumans, Marie-Jose, Doevendans, Pieter A., van Echteld, Cees J.A., Joles, Jaap A., Quax, Paul H., Piek, Jan J., Pasterkamp, Gerard, de Kleijn, Dominique P.V.·2008·Circulation Research
DOI 10.1161/circresaha.107.158220
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Abstract

Left ventricular (LV) remodeling leads to congestive heart failure and is a main determinant of morbidity and mortality following myocardial infarction. Therapeutic options to prevent LV remodeling are limited, which necessitates the exploration of alternative therapeutic targets. Toll-like receptors (TLRs) serve as pattern recognition receptors within the innate immune system. Activation of TLR4 results in an inflammatory response and is involved in extracellular matrix degradation, both key processes of LV remodeling following myocardial infarction. To establish the role of TLR4 in postinfarct LV remodeling, myocardial infarction was induced in wild-type BALB/c mice and TLR4-defective C3H- Tlr4 LPS−d mice. Without affecting infarct size, TLR4 defectiveness reduced the extent of LV remodeling (end-diastolic volume: 103.7±6.8 μL versus 128.5±5.7 μL; P <0.01) and preserved systolic function (ejection fraction: 28.2±3.1% versus 16.6±1.3%; P <0.01), as assessed by MRI. In the noninfarcted area, interstitial fibrosis, and myocardial hypertrophy were reduced in C3H- Tlr4 LPS−d mice. In the infarcted area, however, collagen density was increased, which was accompanied by fewer macrophages, reduced inflammation regulating cytokine expression levels (interleukin [IL]-1α, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, tumor necrosis factor-α, interferon-γ, granulocyte/macrophage colony-stimulating factor), and reduced matrix metalloproteinase-2 (4684±515 versus 7573±611; P =0.002) and matrix metalloproteinase-9 activity (76.0±14.3 versus 168.0±36.2; P =0.027). These data provide direct evidence for a causal role of TLR4 in postinfarct maladaptive LV remodeling, probably via inflammatory cytokine production and matrix degradation. TLR4 may therefore constitute a novel target in the treatment of ischemic heart failure.

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Metadata

Authors
Timmers, L., Sluijter, J. P. G., van Keulen, J. K., Hoefer, I. E., Nederhoff, M. G. J., Goumans, M.-J., Doevendans, P. A., van Echteld, C. J. A., Joles, J. A., Quax, P. H., Piek, J. J., Pasterkamp, G., & de Kleijn, D. P. V.
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2008-02
Volume
102
Issue
2
Pages
257-264
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/circresaha.107.158220
OpenAlex
W2145655023
Cited by
344
References
32
FWCI
10.80
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Toll-Like Receptor 4 Mediates Maladaptive Left Ventricular Remodeling and Impairs Cardiac Function After Myocardial Infarction. https://app.cochat.ai/papers/10.1161/circresaha.107.158220
The paper
Timmers, L., Sluijter, J. P. G., van Keulen, J. K., Hoefer, I. E., Nederhoff, M. G. J., Goumans, M.-J., Doevendans, P. A., van Echteld, C. J. A., Joles, J. A., Quax, P. H., Piek, J. J., Pasterkamp, G., & de Kleijn, D. P. V. (2008). Toll-Like Receptor 4 Mediates Maladaptive Left Ventricular Remodeling and Impairs Cardiac Function After Myocardial Infarction. Circulation Research. https://doi.org/10.1161/circresaha.107.158220

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.