Abstract
For many years elastin was considered as the matrix component structurally required to provide tissue elasticity. However, the expanded knowledge on the regulation of connective tissue homeostasis has revealed that elastic fibers also represent a source of elastokines and are the target of a number of signaling pathways mainly involving the TGF-β/BMP axis. A better understanding of these complex regulatory networks may pave the way for targeted therapeutic strategies in a number of genetic as well as acquired diseases and for the development of new functionalized biomaterials.
Highlights
For many years elastin was considered as the matrix component structurally required to provide tissue elasticity
Elastic fibers are principally composed of a crosslinked elastin core deposited on a scaffold of fibrillin-rich microfibrils which requires, for its initial formation, the assembly of fibronectin molecules [3]
To be noted is that the soluble precursor tropoelastin is deposited onto microfibrils with the help of many other matrix components such as proteoglycans [4,5], fibulins 4 and 5 [6], as well as latent TGF-β binding protein-4 [7]
Summary
For many years elastin was considered as the matrix component structurally required to provide tissue elasticity. It has been demonstrated that elastic fiber degradation can release elastin fragments named elastokines due to their cytokinelike signaling properties [15], as they exhibit potent chemotactic activities for leukocytes, stimulate fibroblast and smooth muscle cell proliferation and display proangiogenic activity, sustaining the use of these peptides, as substitutes of the whole molecule, for bioengineering applications [16], including the generation of bio-inspired materials based on the repetitive sequence XGGZG (X,Z = V,L or A) forming amyloid-like nanostructures [17,18].
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