Abstract
A wide range of environmental factors (e.g. UV radiation, pollution) challenges skin homeostasis and its prolonged imbalance accelerates skin aging. Aged skin is characterized by presence of senescent cells, which have a changed appearance and phenotype, accumulate damaged biomolecules and simultaneously produce a mixture of danger signaling molecules which negatively affect their microenvironment and activate the immune response. We previously described increased levels of lysophosphatidylcholines, in both replicative senescent and in in vitro stress-induced premature senescent (SIPS) fibroblasts.
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