@misc{MuenchAbdelilahSeyfried2021,
  author    = {M{\"u}nch, Juliane and Abdelilah-Seyfried, Salim},
  title     = {Sensing and Responding of Cardiomyocytes to Changes of Tissue Stiffness in the Diseased Heart},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-54580},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-545805},
  pages     = {15},
  year      = {2021},
  abstract  = {Cardiomyocytes are permanently exposed to mechanical stimulation due to cardiac contractility. Passive myocardial stiffness is a crucial factor, which defines the physiological ventricular compliance and volume of diastolic filling with blood. Heart diseases often present with increased myocardial stiffness, for instance when fibrotic changes modify the composition of the cardiac extracellular matrix (ECM). Consequently, the ventricle loses its compliance, and the diastolic blood volume is reduced. Recent advances in the field of cardiac mechanobiology revealed that disease-related environmental stiffness changes cause severe alterations in cardiomyocyte cellular behavior and function. Here, we review the molecular mechanotransduction pathways that enable cardiomyocytes to sense stiffness changes and translate those into an altered gene expression. We will also summarize current knowledge about when myocardial stiffness increases in the diseased heart. Sophisticated in vitro studies revealed functional changes, when cardiomyocytes faced a stiffer matrix. Finally, we will highlight recent studies that described modulations of cardiac stiffness and thus myocardial performance in vivo. Mechanobiology research is just at the cusp of systematic investigations related to mechanical changes in the diseased heart but what is known already makes way for new therapeutic approaches in regenerative biology.},
  language  = {en}
}
@article{MuenchAbdelilahSeyfried2021,
  author    = {M{\"u}nch, Juliane and Abdelilah-Seyfried, Salim},
  title     = {Sensing and responding of cardiomyocytes to changes of tissue stiffness in the diseased heart},
  series = {Frontiers in cell developmental biology},
  volume    = {9},
  journal   = {Frontiers in cell developmental biology},
  publisher = {Frontiers Media},
  address   = {Lausanne},
  issn      = {2296-634X},
  doi       = {10.3389/fcell.2021.642840},
  pages     = {13},
  year      = {2021},
  abstract  = {Cardiomyocytes are permanently exposed to mechanical stimulation due to cardiac contractility. Passive myocardial stiffness is a crucial factor, which defines the physiological ventricular compliance and volume of diastolic filling with blood. Heart diseases often present with increased myocardial stiffness, for instance when fibrotic changes modify the composition of the cardiac extracellular matrix (ECM). Consequently, the ventricle loses its compliance, and the diastolic blood volume is reduced. Recent advances in the field of cardiac mechanobiology revealed that disease-related environmental stiffness changes cause severe alterations in cardiomyocyte cellular behavior and function. Here, we review the molecular mechanotransduction pathways that enable cardiomyocytes to sense stiffness changes and translate those into an altered gene expression. We will also summarize current knowledge about when myocardial stiffness increases in the diseased heart. Sophisticated in vitro studies revealed functional changes, when cardiomyocytes faced a stiffer matrix. Finally, we will highlight recent studies that described modulations of cardiac stiffness and thus myocardial performance in vivo. Mechanobiology research is just at the cusp of systematic investigations related to mechanical changes in the diseased heart but what is known already makes way for new therapeutic approaches in regenerative biology.},
  language  = {en}
}
@misc{MacGroganMuenchdelaPompa2018,
  author    = {MacGrogan, Donal and M{\"u}nch, Juliane and de la Pompa, Jos{\´e} Luis},
  title     = {Notch and interacting signalling pathways in cardiac development, disease, and regeneration},
  series = {Nature Reviews Cardiology},
  volume    = {15},
  journal   = {Nature Reviews Cardiology},
  number    = {11},
  publisher = {Nature Publ. Group},
  address   = {New York},
  issn      = {1759-5002},
  doi       = {10.1038/s41569-018-0100-2},
  pages     = {685 -- 704},
  year      = {2018},
  abstract  = {Cardiogenesis is a complex developmental process involving multiple overlapping stages of cell fate specification, proliferation, differentiation, and morphogenesis. Precise spatiotemporal coordination between the different cardiogenic processes is ensured by intercellular signalling crosstalk and tissue-tissue interactions. Notch is an intercellular signalling pathway crucial for cell fate decisions during multicellular organismal development and is aptly positioned to coordinate the complex signalling crosstalk required for progressive cell lineage restriction during cardiogenesis. In this Review, we describe the role of Notch signalling and the crosstalk with other signalling pathways during the differentiation and patterning of the different cardiac tissues and in cardiac valve and ventricular chamber development. We examine how perturbation of Notch signalling activity is linked to congenital heart diseases affecting the neonate and adult, and discuss studies that shed light on the role of Notch signalling in heart regeneration and repair after injury.},
  language  = {en}
}
@article{AndresDelgadoErnstGalardiCastillaetal.2019,
  author    = {Andr{\´e}s-Delgado, Laura and Ernst, Alexander and Galardi-Castilla, Mar{\´i}a and Bazaga, David and Peralta, Marina and M{\"u}nch, Juliane and Gonzalez-Rosa, Juan M. and Marques, In{\^e}s and Tessadori, Federico and de la Pompa, Jos{\´e} Luis and Vermot, Julien and Mercader, Nadia},
  title     = {Actin dynamics and the Bmp pathway drive apical extrusion of proepicardial cells},
  series = {Development : Company of Biologists},
  volume    = {146},
  journal   = {Development : Company of Biologists},
  number    = {13},
  publisher = {The Company of Biologists Ltd},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.174961},
  pages     = {15},
  year      = {2019},
  abstract  = {The epicardium, the outer mesothelial layer enclosing the myocardium, plays key roles in heart development and regeneration. During embryogenesis, the epicardium arises from the proepicardium (PE), a cell cluster that appears in the dorsal pericardium (DP) close to the venous pole of the heart. Little is known about how the PE emerges from the pericardial mesothelium. Using a zebrafish model and a combination of genetic tools, pharmacological agents and quantitative in vivo imaging, we reveal that a coordinated collective movement of DP cells drives PE formation. We found that Bmp signaling and the actomyosin cytoskeleton promote constriction of the DP, which enables PE cells to extrude apically. We provide evidence that cell extrusion, which has been described in the elimination of unfit cells from epithelia and the emergence of hematopoietic stem cells, is also a mechanism for PE cells to exit an organized mesothelium and fulfil their developmental fate to form a new tissue layer, the epicardium.},
  language  = {en}
}