The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia–reperfusion injury
Abstract
AIMS: Nucleotide-binding oligomerization domain-Like Receptor with a Pyrin domain 3 (NLRP3) is considered necessary for initiating a profound sterile inflammatory response. NLRP3 forms multi-protein complexes with Apoptosis-associated Speck-like protein containing a Caspase recruitment domain (ASC) and Caspase-1, which activate pro-interleukin-1β (IL-1β) and pro-IL-18. The role of NLRP3 in cardiac cells is not known. Thus, we investigated the expression and function of NLRP3 during myocardial ischaemia. METHODS AND RESULTS: Myocardial infarction (MI) was induced in adult C57BL/6 mice and Wistar rats by ligation of the coronary artery. A marked increase in NLRP3, IL-1β, and IL-18 mRNA expression was found in the left ventricle after MI, primarily located to myocardial fibroblasts. In vitro studies in cells from adult mice showed that myocardial fibroblasts released IL-1β and IL-18 when primed with lipopolysaccharide and subsequently exposed to the danger signal adenosine triphosphate, a molecule released after tissue damage during MI. When hearts were isolated from NLRP3-deficient mice, perfused and subjected to global ischaemia and reperfusion, a marked improvement of cardiac function and reduction of hypoxic damage was found compared with wild-type hearts. This was not observed in ASC-deficient hearts, potentially reflecting a protective role of other ASC-dependent inflammasomes or inflammasome-independent effects of NLRP3. CONCLUSION: This study shows that the NLRP3 inflammasome is up-regulated in myocardial fibroblasts post-MI, and may be a significant contributor to infarct size development during ischaemia-reperfusion.
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Cites
Functional interactions between the gut microbiota and host metabolism
Tremaroli, V., & Bäckhed, F. (2012) · Nature · doi:10.1038/nature11552 · Cited by 4,387
Immunological and inflammatory functions of the interleukin-1 family
Dinarello, C. A. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132612 · Cited by 3,466
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HMGB1 SIGNALS THROUGH TOLL-LIKE RECEPTOR (TLR) 4 AND TLR2
Yu, M., Wang, H., Ding, A., Golenbock, D. T., Latz, E., Czura, C. J., Fenton, M. J., Tracey, K. J., & Yang, H. (2006) · Shock · doi:10.1097/01.shk.0000225404.51320.82 · Cited by 832
Cited by
Targeting the NLRP3 inflammasome in inflammatory diseases
Mangan, M. S. J., Olhava, E. J., Roush, W. R., Seidel, H. M., Glick, G. D., & Latz, E. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.97 · Cited by 1,885
Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease
Del Re, D. P., Amgalan, D., Linkermann, A., Liu, Q., & Kitsis, R. N. (2019) · Physiological Reviews · doi:10.1152/physrev.00022.2018 · Cited by 961
NLRP3 inflammasome and its inhibitors: a review
Shao, B.-Z., Xu, Z.-Q., Han, B.-Z., Su, D.-F., & Liu, C. (2015) · Frontiers in Pharmacology · doi:10.3389/fphar.2015.00262 · Cited by 836
“…models, studies have also defined a role for the NLRP3 inflammasome in the initiation and development of cerebral and myocardial ischemic diseases, including cerebral ischemia/stroke and myocardial ischemia (Sandanger et al., 2013; Marchetti et al., 2014; Hecker et al., 2015; Ito et al., 2015).”
BackgroundFibroblasts in myocardial infarction: A role in inflammation and repair
Shinde, A. V., & Frangogiannis, N. G. (2014) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.11.015 · Cited by 522
Regulated cell death in myocardial ischemia–reperfusion injury
Xiang, Q., Yi, X., Zhu, X.-H., Wei, X., & Jiang, D.-S. (2024) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2023.10.010 · Cited by 448
Metadata
- Authors
- Sandanger, Ø., Ranheim, T., Vinge, L. E., Bliksøen, M., Alfsnes, K., Finsen, A. V., Dahl, C. P., Askevold, E. T., Florholmen, G., Christensen, G., Fitzgerald, K. A., Lien, E., Valen, G., Espevik, T., Aukrust, P., & Yndestad, A.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-04-10
- Volume
- 99
- Issue
- 1
- Pages
- 164-174
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- OpenAlex
- W2170168704
- Cited by
- 524
- References
- 4
- FWCI
- 13.18
- Type
- journal article
- Language
- en
- Open access
- closed
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- Sandanger, Ø., Ranheim, T., Vinge, L. E., Bliksøen, M., Alfsnes, K., Finsen, A. V., Dahl, C. P., Askevold, E. T., Florholmen, G., Christensen, G., Fitzgerald, K. A., Lien, E., Valen, G., Espevik, T., Aukrust, P., & Yndestad, A. (2013). The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia–reperfusion injury. Cardiovascular Research. https://doi.org/10.1093/cvr/cvt091
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