Human skin is largely composed of a collagen-rich connective tissue, which provides structural and functional support. This connective tissue which is the dermal extracellular matrix (ECM) produced, organized, and maintained by dermal fibroblasts and confers strength and resiliency to skin. In young skin, fibroblasts produce and adhere to the dermal ECM. Adherence allows fibroblasts to spread and exert mechanical force on the surrounding ECM. In this state, fibroblasts display a “youthful” phenotype characterized by maintenance of the composition and structural organization of the dermal ECM. During aging, fibroblast-ECM interactions become disrupted due to fragmentation of collagen fibrils. This disruption causes loss of fibroblast spreading and mechanical force, which inextricably lead to an “aged” phenotype; fibroblasts synthesize less ECM proteins and more matrix-degrading metalloproteinases. This imbalance of ECM homeostasis further drives collagen fibril fragmentation in a self-perpetuating cycle. Age-related alterations of collagen fibrils impairs skin structure and function and creates a tissue microenvironment that promotes age-related skin diseases, such as delayed wound healing and skin cancer development (Cole et al., 2018), (Quan and Fisher, 2015).
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