The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension
Open accessAbstract
Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible changes to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Laurent, S., Boutouyrie, P., Asmar, R., Gautier, I., Laloux, B., Guize, L., Ducimetiere, P., & Benetos, A. (2001) · Hypertension · doi:10.1161/01.hyp.37.5.1236 · Cited by 3,856
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K., & Hauser, C. J. (2010) · Nature · doi:10.1038/nature08780 · Cited by 3,812
The two NF-κB activation pathways and their role in innate and adaptive immunity
Bonizzi, G., & Karin, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.03.008 · Cited by 2,535
Metabolic Syndrome and Altered Gut Microbiota in Mice Lacking Toll-Like Receptor 5
Vijay-Kumar, M., Aitken, J. D., Carvalho, F. A., Cullender, T. C., Mwangi, S., Srinivasan, S., Sitaraman, S. V., Knight, R., Ley, R. E., & Gewirtz, A. T. (2010) · Science · doi:10.1126/science.1179721 · Cited by 2,068
Immunological memory and protective immunity: understanding their relation
Ahmed, R., & Gray, D. (1996) · Science · doi:10.1126/science.272.5258.54 · Cited by 1,775 · cited 1×
“Proliferation and differentiation of naive lymphocytes into effector cells is necessary for elimination of the antigen and production of memory cells, which protect the host upon subsequent encounters with the antigen (3).”
Physiological aspects of primary hypertension.
Folkow, B. (1982) · Physiological Reviews · doi:10.1152/physrev.1982.62.2.347 · Cited by 1,768
Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Guzik, T. J., Hoch, N. E., Brown, K. A., McCann, L. A., Rahman, A., Dikalov, S., Goronzy, J., Weyand, C., & Harrison, D. G. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070657 · Cited by 1,736
Regulation of lung injury and repair by Toll-like receptors and hyaluronan
Jiang, D., Liang, J., Fan, J., Yu, S., Chen, S., Luo, Y., Prestwich, G. D., Mascarenhas, M. M., Garg, H. G., Quinn, D. A., et al. (2005) · Nature Medicine · doi:10.1038/nm1315 · Cited by 1,401
Gene-specific control of inflammation by TLR-induced chromatin modifications
Foster, S. L., Hargreaves, D. C., & Medzhitov, R. (2007) · Nature · doi:10.1038/nature05836 · Cited by 1,344
Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure
Oka, T., Hikoso, S., Yamaguchi, O., Taneike, M., Takeda, T., Tamai, T., Oyabu, J., Murakawa, T., Nakayama, H., Nishida, K., et al. (2012) · Nature · doi:10.1038/nature10992 · Cited by 1,201
Cited by
Denning, N.-L., Aziz, M., Gurien, S. D., & Wang, P. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02536 · Cited by 623
Wanderley, C. W., Colón, D. F., Luiz, J. P. M., Oliveira, F. F., Viacava, P. R., Leite, C. A., Pereira, J. A., Silva, C. M., Silva, C. R., Silva, R. L., et al. (2018) · Cancer Research · doi:10.1158/0008-5472.can-17-3480 · Cited by 420
Role of the Immune System in Hypertension
Rodriguez-Iturbe, B., Pons, H., & Johnson, R. J. (2017) · Physiological Reviews · doi:10.1152/physrev.00031.2016 · Cited by 391
Gao, W., Xiong, Y., Li, Q., & Yang, H. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00508 · Cited by 353
The immune system and hypertension
Singh, M. V., Chapleau, M. W., Harwani, S. C., & Abboud, F. M. (2014) · Immunologic Research · doi:10.1007/s12026-014-8548-6 · Cited by 176
Metadata
- Authors
- McCarthy, C. G., Goulopoulou, S., Wenceslau, C. F., Spitler, K., Matsumoto, T., & Webb, R. C.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2014-01-15
- Volume
- 306
- Issue
- 2
- Pages
- H184-H196
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2169848995
- Cited by
- 182
- References
- 16
- FWCI
- 7.39
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension. https://app.cochat.ai/papers/10.1152/ajpheart.00328.2013
- The paper
- McCarthy, C. G., Goulopoulou, S., Wenceslau, C. F., Spitler, K., Matsumoto, T., & Webb, R. C. (2014). Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00328.2013
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.