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Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation.

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Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation. / Rudolph, Volker; Andrié, René P; Rudolph, Tanja Katharina; Friedrichs, Kai; Klinke, Anna; Hirsch-Hoffmann, Birgit; Schwoerer, Alexander; Lau, Denise; Fu, Xiaoming; Klingel, Karin; Sydow, Karsten; Didié, Michael; Seniuk, Anika; von Leitner, Eike-Christin; Szöcs, Katalin; Schrickel, Jan W; Treede, Hendrik; Wenzel, Ulrich; Lewalter, Thorsten; Nickenig, Georg; Zimmermann, Wolfram-Hubertus; Meinertz, Thomas; Böger, Rainer; Reichenspurner, Hermann; Freeman, Bruce A; Eschenhagen, Thomas; Ehmke, Heimo; Hazen, Stanley L; Willems, Stephan; Baldus, Stephan.

in: NAT MED, Jahrgang 16, Nr. 4, 4, 2010, S. 470-474.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Rudolph, V, Andrié, RP, Rudolph, TK, Friedrichs, K, Klinke, A, Hirsch-Hoffmann, B, Schwoerer, A, Lau, D, Fu, X, Klingel, K, Sydow, K, Didié, M, Seniuk, A, von Leitner, E-C, Szöcs, K, Schrickel, JW, Treede, H, Wenzel, U, Lewalter, T, Nickenig, G, Zimmermann, W-H, Meinertz, T, Böger, R, Reichenspurner, H, Freeman, BA, Eschenhagen, T, Ehmke, H, Hazen, SL, Willems, S & Baldus, S 2010, 'Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation.', NAT MED, Jg. 16, Nr. 4, 4, S. 470-474. https://doi.org/10.1038/nm.2124

APA

Rudolph, V., Andrié, R. P., Rudolph, T. K., Friedrichs, K., Klinke, A., Hirsch-Hoffmann, B., Schwoerer, A., Lau, D., Fu, X., Klingel, K., Sydow, K., Didié, M., Seniuk, A., von Leitner, E-C., Szöcs, K., Schrickel, J. W., Treede, H., Wenzel, U., Lewalter, T., ... Baldus, S. (2010). Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation. NAT MED, 16(4), 470-474. [4]. https://doi.org/10.1038/nm.2124

Vancouver

Rudolph V, Andrié RP, Rudolph TK, Friedrichs K, Klinke A, Hirsch-Hoffmann B et al. Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation. NAT MED. 2010;16(4):470-474. 4. https://doi.org/10.1038/nm.2124

Bibtex

@article{46e607d7efb74b068a5158a89d564bfc,
title = "Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation.",
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.",
author = "Volker Rudolph and Andri{\'e}, {Ren{\'e} P} and Rudolph, {Tanja Katharina} and Kai Friedrichs and Anna Klinke and Birgit Hirsch-Hoffmann and Alexander Schwoerer and Denise Lau and Xiaoming Fu and Karin Klingel and Karsten Sydow and Michael Didi{\'e} and Anika Seniuk and {von Leitner}, Eike-Christin and Katalin Sz{\"o}cs and Schrickel, {Jan W} and Hendrik Treede and Ulrich Wenzel and Thorsten Lewalter and Georg Nickenig and Wolfram-Hubertus Zimmermann and Thomas Meinertz and Rainer B{\"o}ger and Hermann Reichenspurner and Freeman, {Bruce A} and Thomas Eschenhagen and Heimo Ehmke and Hazen, {Stanley L} and Stephan Willems and Stephan Baldus",
year = "2010",
doi = "10.1038/nm.2124",
language = "Deutsch",
volume = "16",
pages = "470--474",
journal = "NAT MED",
issn = "1078-8956",
publisher = "NATURE PUBLISHING GROUP",
number = "4",

}

RIS

TY - JOUR

T1 - Myeloperoxidase acts as a profibrotic mediator of atrial fibrillation.

AU - Rudolph, Volker

AU - Andrié, René P

AU - Rudolph, Tanja Katharina

AU - Friedrichs, Kai

AU - Klinke, Anna

AU - Hirsch-Hoffmann, Birgit

AU - Schwoerer, Alexander

AU - Lau, Denise

AU - Fu, Xiaoming

AU - Klingel, Karin

AU - Sydow, Karsten

AU - Didié, Michael

AU - Seniuk, Anika

AU - von Leitner, Eike-Christin

AU - Szöcs, Katalin

AU - Schrickel, Jan W

AU - Treede, Hendrik

AU - Wenzel, Ulrich

AU - Lewalter, Thorsten

AU - Nickenig, Georg

AU - Zimmermann, Wolfram-Hubertus

AU - Meinertz, Thomas

AU - Böger, Rainer

AU - Reichenspurner, Hermann

AU - Freeman, Bruce A

AU - Eschenhagen, Thomas

AU - Ehmke, Heimo

AU - Hazen, Stanley L

AU - Willems, Stephan

AU - Baldus, Stephan

PY - 2010

Y1 - 2010

N2 - 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.

AB - 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.

U2 - 10.1038/nm.2124

DO - 10.1038/nm.2124

M3 - SCORING: Zeitschriftenaufsatz

VL - 16

SP - 470

EP - 474

JO - NAT MED

JF - NAT MED

SN - 1078-8956

IS - 4

M1 - 4

ER -