@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}
}
@article{BornhorstAbdelilahSeyfried2021,
  author    = {Bornhorst, Dorothee and Abdelilah-Seyfried, Salim},
  title     = {Strong as a Hippo's Heart: Biomechanical Hippo Signaling During Zebrafish Cardiac Development},
  series = {Frontiers in Cell and Developmental Biology},
  volume    = {9},
  journal   = {Frontiers in Cell and Developmental Biology},
  publisher = {Frontiers Media},
  address   = {Lausanne, Schweiz},
  issn      = {2296-634X},
  doi       = {10.3389/fcell.2021.731101},
  pages     = {1 -- 10},
  year      = {2021},
  abstract  = {The heart is comprised of multiple tissues that contribute to its physiological functions. During development, the growth of myocardium and endocardium is coupled and morphogenetic processes within these separate tissue layers are integrated. Here, we discuss the roles of mechanosensitive Hippo signaling in growth and morphogenesis of the zebrafish heart. Hippo signaling is involved in defining numbers of cardiac progenitor cells derived from the secondary heart field, in restricting the growth of the epicardium, and in guiding trabeculation and outflow tract formation. Recent work also shows that myocardial chamber dimensions serve as a blueprint for Hippo signaling-dependent growth of the endocardium. Evidently, Hippo pathway components act at the crossroads of various signaling pathways involved in embryonic zebrafish heart development. Elucidating how biomechanical Hippo signaling guides heart morphogenesis has direct implications for our understanding of cardiac physiology and pathophysiology.},
  language  = {en}
}
@article{RoedelAbdelilahSeyfried2021,
  author    = {R{\"o}del, Claudia Jasmin and Abdelilah-Seyfried, Salim},
  title     = {A zebrafish toolbox for biomechanical signaling in cardiovascular development and disease},
  series = {Current opinion in hematology},
  volume    = {28},
  journal   = {Current opinion in hematology},
  number    = {3},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {1065-6251},
  doi       = {10.1097/MOH.0000000000000648},
  pages     = {198 -- 207},
  year      = {2021},
  abstract  = {Purpose of review The zebrafish embryo has emerged as a powerful model organism to investigate the mechanisms by which biophysical forces regulate vascular and cardiac cell biology during development and disease. A versatile arsenal of methods and tools is available to manipulate and analyze biomechanical signaling. This review aims to provide an overview of the experimental strategies and tools that have been utilized to study biomechanical signaling in cardiovascular developmental processes and different vascular disease models in the zebrafish embryo. Within the scope of this review, we focus on work published during the last two years. Recent findings Genetic and pharmacological tools for the manipulation of cardiac function allow alterations of hemodynamic flow patterns in the zebrafish embryo and various types of transgenic lines are available to report endothelial cell responses to biophysical forces. These tools have not only revealed the impact of biophysical forces on cardiovascular development but also helped to establish more accurate models for cardiovascular diseases including cerebral cavernous malformations, hereditary hemorrhagic telangiectasias, arteriovenous malformations, and lymphangiopathies. Summary The zebrafish embryo is a valuable vertebrate model in which in-vivo manipulations of biophysical forces due to cardiac contractility and blood flow can be performed. These analyses give important insights into biomechanical signaling pathways that control endothelial and endocardial cell behaviors. The technical advances using this vertebrate model will advance our understanding of the impact of biophysical forces in cardiovascular pathologies.},
  language  = {en}
}