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Korf-Klingebiel M, Reboll MR, Polten F, et al. Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca. Circulation. 2021;144(15):1227-1240doi: 10.1161/CIRCULATIONAHA.120.053365.
Korf-Klingebiel, M., Reboll, M. R., Polten, F., Weber, N., Jäckle, F., Wu, X., Kallikourdis, M., Kunderfranco, P., Condorelli, G., Giannitsis, E., Kustikova, O. S., Schambach, A., Pich, A., Widder, J. D., Bauersachs, J., van den Heuvel, J., Kraft, T., Wang, Y., & Wollert, K. C. (2021). Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca. Circulation, 144(15), 1227-1240. https://doi.org/10.1161/CIRCULATIONAHA.120.053365
Korf-Klingebiel, Mortimer, et al. "Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca." Circulation vol. 144,15 (2021): 1227-1240. doi: https://doi.org/10.1161/CIRCULATIONAHA.120.053365
Korf-Klingebiel M, Reboll MR, Polten F, Weber N, Jäckle F, Wu X, Kallikourdis M, Kunderfranco P, Condorelli G, Giannitsis E, Kustikova OS, Schambach A, Pich A, Widder JD, Bauersachs J, van den Heuvel J, Kraft T, Wang Y, Wollert KC. Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca. Circulation. 2021 Oct 12;144(15):1227-1240. doi: 10.1161/CIRCULATIONAHA.120.053365. Epub 2021 Aug 10. PMID: 34372689.
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Circulation. 2021 Oct 12;144(15):1227-1240. doi: 10.1161/CIRCULATIONAHA.120.053365. Epub 2021 Aug 10.

Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca.

Circulation

Mortimer Korf-Klingebiel, Marc R Reboll, Felix Polten, Natalie Weber, Felix Jäckle, Xuekun Wu, Marinos Kallikourdis, Paolo Kunderfranco, Gianluigi Condorelli, Evangelos Giannitsis, Olga S Kustikova, Axel Schambach, Andreas Pich, Julian D Widder, Johann Bauersachs, Joop van den Heuvel, Theresia Kraft, Yong Wang, Kai C Wollert

Affiliations

  1. Division of Molecular and Translational Cardiology, Department of Cardiology and Angiology (M.K.-K., M.R.R., F.P., F.J., X.W., Y.W., K.C.W.).
  2. Institute for Molecular and Cellular Physiology (N.W., T.K.).
  3. Humanitas Clinical and Research Center IRCCS, Rozzano, Milan, Italy (M.K., P.K., G.C.).
  4. Humanitas University, Pieve Emanuele, Milan, Italy (M.K., G.C.).
  5. Department of Medicine III, University of Heidelberg, Germany (E.G.).
  6. Institute of Experimental Hematology (O.S.K., A.S.).
  7. Core Unit Proteomics and Institute of Toxicology (A.P.), Hannover Medical School, Germany.
  8. Department of Cardiology and Angiology (J.D.W., J.B.).
  9. Technology Platform Recombinant Protein Expression, Helmholtz Center for Infection Research, Braunschweig, Germany (J.v.d.H.).

PMID: 34372689 DOI: 10.1161/CIRCULATIONAHA.120.053365

Abstract

BACKGROUND: Inflammation contributes to the pathogenesis of heart failure, but there is limited understanding of inflammation's potential benefits. Inflammatory cells secrete MYDGF (myeloid-derived growth factor) to promote tissue repair after acute myocardial infarction. We hypothesized that MYDGF has a role in cardiac adaptation to persistent pressure overload.

METHODS: We defined the cellular sources and function of MYDGF in wild-type (WT),

RESULTS: MYDGF protein abundance increased in the left ventricular myocardium and in blood plasma of pressure-overloaded mice. Patients with severe aortic stenosis also had elevated MYDGF plasma concentrations, which declined after transcatheter aortic valve implantation. Monocytes and macrophages emerged as the main MYDGF sources in the pressure-overloaded murine heart. While

CONCLUSIONS: These findings establish a MYDGF-based adaptive crosstalk between inflammatory cells and cardiomyocytes that protects against pressure overload-induced heart failure.

Keywords: heart failure; inflammation; intercellular signaling peptides and proteins; myocytes, cardiac; sarcoplasmic reticulum calcium-transporting ATPases

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