Nature Communications (Jan 2022)

Skeletal muscle derived Musclin protects the heart during pathological overload

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

DOI
https://doi.org/10.1038/s41467-021-27634-5
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 17

Abstract

Read online

Cachexia is associated with poor prognosis in heart failure. Here the authors show that mice and patients with cardiac cachexia display reduced skeletal muscle expression and circulating levels of Musclin. Musclin ablation in skeletal muscle worsens, while its muscle-specific overexpression ameliorates heart failure in mice.