According to this article:
Cardiac scars, often perceived as “dead” tissue, are very much alive, with heterocellular activity ensuring the maintenance of structural and mechanical integrity following heart injury. To form a scar, non-myocytes such as fibroblasts, proliferate and are recruited from intra- and extra-cardiac sources. Fibroblasts perform important autocrine and paracrine signalling functions. They also establish mechanical and, as is increasingly evident, electrical junctions with other cells. While fibroblasts were previously thought to act simply as electrical insulators, they may be electrically connected among themselves and, under certain circumstances, to other cells, including cardiomyocytes. A better understanding of these interactions will help target scar structure and function and facilitate the development of novel therapies aimed at modifying scar properties for patient benefit.
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Fibrotic scars, such as in skin, are generally acellular and predominantly composed of fibrillar collagen [11]. In the heart, however, scar tissue assumes a more proactive role than simply preserving ventricular integrity, facilitating force transmission, and preventing rupture. Nonetheless, myocardial scarring does share common mechanisms and morphological milestones with classic wound healing.
Despite prevailing perceptions, cardiac scars are dynamic living structures [16, 17]. The abundantly present ECM is interlaced with phenotypically diverse groups of cells: interstitial fibroblast-like cells (both functionally and structurally heterogeneous, endothelial cells, vascular smooth muscle, surviving cardiomyocytes, immune cells, neurons, and adipocytes [18, 19] (Fig. 1B,C). The scar is a metabolically dynamic tissue which furthermore, exhibits non-linear passive and active mechanical properties (‘active’ force-generation by non-myocytes over time occurs at scales that are orders of magnitude longer than the heartbeat) [20]. Contractile properties of the scar rely on the presence of non-vascular, α-smooth muscle actin-expressing non-myocytes, which persist in cardiac scars for many years following injury, such as with myocardial infarction (MI) [21–23] (note that not all subsets of fibroblasts express contractile proteins [24]). They also depend on the presence of an extensive cytoplasmic fibrillar system of cell-to-cell and cell-to-ECM attachments [25].
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