Abstract
Skin undergoes continuous renewal throughout an individual’s lifetime relying on stem cell functionality. However, a decline of the skin regenerative potential occurs with age. The accumulation of senescent cells over time probably reduces tissue regeneration and contributes to skin aging. Keratinocytes and dermal fibroblasts undergo senescence in response to several intrinsic or extrinsic stresses, including telomere shortening, overproduction of reactive oxygen species, diet, and sunlight exposure. Epigenetic mechanisms directly regulate skin homeostasis and regeneration, but they also mark cell senescence and the natural and pathological aging processes. Progeroid syndromes represent a group of clinical and genetically heterogeneous pathologies characterized by the accelerated aging of various tissues and organs, including skin. Skin cells from progeroid patients display molecular hallmarks that mimic those associated with naturally occurring aging. Thus, investigations on progeroid syndromes strongly contribute to disclose the causal mechanisms that underlie the aging process. In the present review, we discuss the role of epigenetic pathways in skin cell regulation during physiologic and premature aging.
Highlights
The skin protects the body from environmental stresses, such as water loss and microorganism infection, and is made up of three tissue layers: the epidermis, the dermis, and the hypodermis (Figure 1) [1].The human epidermis consists of four major cell layers composed of keratinocytes in stages of progressive differentiation [2]
Even though the activity of hypodermal adipocytes is relevant for skin homeostasis and the separation between the dermal and hypodermal layers is not always well defined [8], the following review will focus on the epigenetic changes and transcriptional regulatory networks associated to an age-dependent functional decline of epidermal Stem cells (SCs) and dermal fibroblasts
During normal skin homeostasis and tissue renewal, epigenetic mechanisms govern the decision between epidermal SC self-renewal and differentiation toward the fully differentiated keratinocytes
Summary
The skin protects the body from environmental stresses, such as water loss and microorganism infection, and is made up of three tissue layers: the epidermis, the dermis, and the hypodermis (Figure 1) [1]. TA-cells withdraw from the cell-cycle and generate post-mitotic keratinocytes that migrate upwards to compose suprabasal and upper layers by executing their terminal differentiation program. This process is tightly regulated by temporal and spatial gene expression modulation. Cells 2018, 7, x; doi: FOR PEER REVIEW www.mdpi.com/journal/cells by three tissue layers: epidermis, dermis, and hypodermis. Even though the activity of hypodermal adipocytes is relevant for skin homeostasis and the separation between the dermal and hypodermal layers is not always well defined [8], the following review will focus on the epigenetic changes and transcriptional regulatory networks associated to an age-dependent functional decline of epidermal SCs and dermal fibroblasts
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