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Extra resources for Cardiac Cytoarchitecture: How to Maintain a Working Heart
During this process, myofibrils are also actively contracting and maturing, suggesting that adhesion remodeling in the heart is dynamic and occurs even while myocytes are shortening and actively pulling against the cell–cell junction. Studies have also shown that cell–cell junction protein increases in cardiac myocytes exposed to cyclic stretch (Zhuang et al. 2000; Salameh et al. 2010), emphasizing the mechanosensitivity of the intercalated disc. Further studies are needed to better understand the role of mechanical forces in intercalated disc assembly and maturation in developing cardiac tissues.
2006; Chaturvedi et al. 2010). Crosstalk between cell– matrix and cell–cell adhesions has been observed in many cell types (Chen 2 In Vitro Tools for Quantifying Structure–Function Relationships in. . 23 et al. 2004; Kim and Asthagiri 2011; Maruthamuthu et al. 2011), suggesting that increased stiffness secondary to fibrosis could induce pathological remodeling of cell–cell adhesions in the heart. To test this, pairs of cardiac myocytes have been cultured on polyacrylamide gels with elastic moduli matching that of a healthy heart and a fibrotic heart (McCain et al.
Each sarcomere consists of interdigitating actin and myosin filaments that slide past each other to shorten the cell and generate contractile forces that sum together to 2 In Vitro Tools for Quantifying Structure–Function Relationships in. . 17 induce organ-level pumping (Boateng and Goldspink 2008). Sarcomeres and myofibrils are highly ordered structures that self-assemble during embryonic and postnatal development by processes that are not well understood, limiting our ability to understand sarcomere dysfunction in disease or replicate mature myofibrillogenesis in engineered cardiac cells and tissues for regenerative medicine.