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Cited by 349

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation

Open access
Rudolph, Volker, Andrié, René P, Rudolph, Tanja K, Friedrichs, Kai, Klinke, Anna, Hirsch-Hoffmann, Birgit, Schwoerer, Alexander P, Lau, Denise, Fu, XiaoMing, Klingel, Karin, Sydow, Karsten, Didié, Michael, Seniuk, Anika, von Leitner, Eike-Christin, Szoecs, Katalin, Schrickel, Jan W, Treede, Hendrik, Wenzel, Ulrich, Lewalter, Thorsten, Nickenig, Georg, Zimmermann, Wolfram-Hubertus, Meinertz, Thomas, Böger, Rainer H, Reichenspurner, Hermann, Freeman, Bruce A, Eschenhagen, Thomas, Ehmke, Heimo, Hazen, Stanley L, Willems, Stephan, Baldus, Stephan·2010·Nature Medicine
DOI 10.1038/nm.2124
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Abstract

Observational clinical and ex vivo studies have established a strong association between atrial fibrillation and inflammation. However, whether inflammation is the cause or the consequence of atrial fibrillation and which specific inflammatory mediators may increase the atria's susceptibility to fibrillation remain elusive. Here we provide experimental and clinical evidence for the mechanistic involvement of myeloperoxidase (MPO), a heme enzyme abundantly expressed by neutrophils, in the pathophysiology of atrial fibrillation. MPO-deficient mice pretreated with angiotensin II (AngII) to provoke leukocyte activation showed lower atrial tissue abundance of the MPO product 3-chlorotyrosine, reduced activity of matrix metalloproteinases and blunted atrial fibrosis as compared to wild-type mice. Upon right atrial electrophysiological stimulation, MPO-deficient mice were protected from atrial fibrillation, which was reversed when MPO was restored. Humans with atrial fibrillation had higher plasma concentrations of MPO and a larger MPO burden in right atrial tissue as compared to individuals devoid of atrial fibrillation. In the atria, MPO colocalized with markedly increased formation of 3-chlorotyrosine. Our data demonstrate that MPO is a crucial prerequisite for structural remodeling of the myocardium, leading to an increased vulnerability to atrial fibrillation.

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Metadata

Authors
Rudolph, V., Andrié, R. P., Rudolph, T. K., Friedrichs, K., Klinke, A., Hirsch-Hoffmann, B., Schwoerer, A. P., Lau, D., Fu, X., Klingel, K., Sydow, K., Didié, M., Seniuk, A., von Leitner, E.-C., Szoecs, K., Schrickel, J. W., Treede, H., Wenzel, U., Lewalter, T., Nickenig, G., Zimmermann, W.-H., Meinertz, T., Böger, R. H., Reichenspurner, H., Freeman, B. A., Eschenhagen, T., Ehmke, H., Hazen, S. L., Willems, S., & Baldus, S.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2010-03-21
Volume
16
Issue
4
Pages
470-474
ISSN
  • 1078-8956 (ISSN-L)
  • 1546-170X
DOI
10.1038/nm.2124
OpenAlex
W1979480120
Cited by
349
References
38
FWCI
11.65
Type
journal article
Language
en
Open access
green

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

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