Abstract
During the postnatal period in mammals, the heart undergoes significant remodeling and cardiac cells progressively lose their embryonic characteristics. At the same time, notable changes in the extracellular matrix (ECM) composition occur with a reduction in the components considered facilitators of cellular proliferation, including fibronectin and periostin, and an increase in collagen fiber organization. Not much is known about the postnatal cardiac fibroblast which is responsible for producing the majority of the ECM, but during the days after birth, mammalian hearts can regenerate after injury with only a transient scar formation. This phenomenon has also been described in adult urodeles and teleosts, but relatively little is known about their cardiac fibroblasts or ECM composition. Here, we review the pre-existing knowledge about cardiac fibroblasts and the ECM during the postnatal period in mammals as well as in regenerative environments.
Highlights
A regeneration continuum exists from invertebrates to vertebrates—planarians can regrow all tissues, amphibians and fish can regenerate limbs and hearts, while adult mammals are capable of wound healing, but in general do not regenerate body parts [1]
Less research effort has been devoted to the cardiac fibroblast, which is essential in the wound healing response and generation of the extracellular matrix (ECM)
Cardiac fibroblasts and the ECM are critical regulators of cardiac organogenesis [8,9], and their interactions with cardiomyocytes, immune cells, and endothelial cells may contribute to the ability to undergo adequate regeneration
Summary
A regeneration continuum exists from invertebrates to vertebrates—planarians can regrow all tissues, amphibians and fish can regenerate limbs and hearts, while adult mammals are capable of wound healing, but in general do not regenerate body parts [1]. In a comparison of embryonic and adult mouse cardiac fibroblasts, higher expression of FN, TNC, collagen genes, and Postn were found in embryonic samples [81] This expression profile was shown to be associated with enhanced cardiomyocyte proliferation providing evidence that both the fibroblasts and the ECM can regulate cardiac regeneration [81]. These studies show that composition of the ECM, consisting of less collagen, with more FN and Postn, facilitates heart regeneration (Table 1) It seems that in mammalian hearts, once the adult ECM is established and the cardiomyocytes have exited the cell cycle, the upregulation of “repairing” ECM constituents, such as FN or TNC, is not enough by itself to induce proliferation, and as a result, a collagenous stiff scar is formed. Further investigation is needed in order to completely define the role and potential therapeutic applications of cardiac fibroblasts and ECM in animal models similar to humans
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