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Skeletal muscle derived Musclin protects the heart during pathological overload

Standard

Skeletal muscle derived Musclin protects the heart during pathological overload. / Szaroszyk, Malgorzata; Kattih, Badder; Martin-Garrido, Abel; Trogisch, Felix A; Dittrich, Gesine M; Grund, Andrea; Abouissa, Aya; Derlin, Katja; Meier, Martin; Holler, Tim; Korf-Klingebiel, Mortimer; Völker, Katharina; Garfias Macedo, Tania; Pablo Tortola, Cristina; Boschmann, Michael; Huang, Nora; Froese, Natali; Zwadlo, Carolin; Malek Mohammadi, Mona; Luo, Xiaojing; Wagner, Michael; Cordero, Julio; Geffers, Robert; Batkai, Sandor; Thum, Thomas; Bork, Nadja; Nikolaev, Viacheslav O; Müller, Oliver J; Katus, Hugo A; El-Armouche, Ali; Kraft, Theresia; Springer, Jochen; Dobreva, Gergana; Wollert, Kai C; Fielitz, Jens; von Haehling, Stephan; Kuhn, Michaela; Bauersachs, Johann; Heineke, Joerg.

in: NAT COMMUN, Jahrgang 13, Nr. 1, 149, 10.01.2022.

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

Harvard

Szaroszyk, M, Kattih, B, Martin-Garrido, A, Trogisch, FA, Dittrich, GM, Grund, A, Abouissa, A, Derlin, K, Meier, M, Holler, T, Korf-Klingebiel, M, Völker, K, Garfias Macedo, T, Pablo Tortola, C, Boschmann, M, Huang, N, Froese, N, Zwadlo, C, Malek Mohammadi, M, Luo, X, Wagner, M, Cordero, J, Geffers, R, Batkai, S, Thum, T, Bork, N, Nikolaev, VO, Müller, OJ, Katus, HA, El-Armouche, A, Kraft, T, Springer, J, Dobreva, G, Wollert, KC, Fielitz, J, von Haehling, S, Kuhn, M, Bauersachs, J & Heineke, J 2022, 'Skeletal muscle derived Musclin protects the heart during pathological overload', NAT COMMUN, Jg. 13, Nr. 1, 149. https://doi.org/10.1038/s41467-021-27634-5

APA

Szaroszyk, M., Kattih, B., Martin-Garrido, A., Trogisch, F. A., Dittrich, G. M., Grund, A., Abouissa, A., Derlin, K., Meier, M., Holler, T., Korf-Klingebiel, M., Völker, K., Garfias Macedo, T., Pablo Tortola, C., Boschmann, M., Huang, N., Froese, N., Zwadlo, C., Malek Mohammadi, M., ... Heineke, J. (2022). Skeletal muscle derived Musclin protects the heart during pathological overload. NAT COMMUN, 13(1), [149]. https://doi.org/10.1038/s41467-021-27634-5

Vancouver

Szaroszyk M, Kattih B, Martin-Garrido A, Trogisch FA, Dittrich GM, Grund A et al. Skeletal muscle derived Musclin protects the heart during pathological overload. NAT COMMUN. 2022 Jan 10;13(1). 149. https://doi.org/10.1038/s41467-021-27634-5

Bibtex

@article{4d39765a5a2841c48480a913645a6fc4,
title = "Skeletal muscle derived Musclin protects the heart during pathological overload",
abstract = "Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.",
author = "Malgorzata Szaroszyk and Badder Kattih and Abel Martin-Garrido and Trogisch, {Felix A} and Dittrich, {Gesine M} and Andrea Grund and Aya Abouissa and Katja Derlin and Martin Meier and Tim Holler and Mortimer Korf-Klingebiel and Katharina V{\"o}lker and {Garfias Macedo}, Tania and {Pablo Tortola}, Cristina and Michael Boschmann and Nora Huang and Natali Froese and Carolin Zwadlo and {Malek Mohammadi}, Mona and Xiaojing Luo and Michael Wagner and Julio Cordero and Robert Geffers and Sandor Batkai and Thomas Thum and Nadja Bork and Nikolaev, {Viacheslav O} and M{\"u}ller, {Oliver J} and Katus, {Hugo A} and Ali El-Armouche and Theresia Kraft and Jochen Springer and Gergana Dobreva and Wollert, {Kai C} and Jens Fielitz and {von Haehling}, Stephan and Michaela Kuhn and Johann Bauersachs and Joerg Heineke",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = jan,
day = "10",
doi = "10.1038/s41467-021-27634-5",
language = "English",
volume = "13",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Skeletal muscle derived Musclin protects the heart during pathological overload

AU - Szaroszyk, Malgorzata

AU - Kattih, Badder

AU - Martin-Garrido, Abel

AU - Trogisch, Felix A

AU - Dittrich, Gesine M

AU - Grund, Andrea

AU - Abouissa, Aya

AU - Derlin, Katja

AU - Meier, Martin

AU - Holler, Tim

AU - Korf-Klingebiel, Mortimer

AU - Völker, Katharina

AU - Garfias Macedo, Tania

AU - Pablo Tortola, Cristina

AU - Boschmann, Michael

AU - Huang, Nora

AU - Froese, Natali

AU - Zwadlo, Carolin

AU - Malek Mohammadi, Mona

AU - Luo, Xiaojing

AU - Wagner, Michael

AU - Cordero, Julio

AU - Geffers, Robert

AU - Batkai, Sandor

AU - Thum, Thomas

AU - Bork, Nadja

AU - Nikolaev, Viacheslav O

AU - Müller, Oliver J

AU - Katus, Hugo A

AU - El-Armouche, Ali

AU - Kraft, Theresia

AU - Springer, Jochen

AU - Dobreva, Gergana

AU - Wollert, Kai C

AU - Fielitz, Jens

AU - von Haehling, Stephan

AU - Kuhn, Michaela

AU - Bauersachs, Johann

AU - Heineke, Joerg

N1 - © 2022. The Author(s).

PY - 2022/1/10

Y1 - 2022/1/10

N2 - Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.

AB - Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.

U2 - 10.1038/s41467-021-27634-5

DO - 10.1038/s41467-021-27634-5

M3 - SCORING: Journal article

C2 - 35013221

VL - 13

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

M1 - 149

ER -