Purpose of review: Systemic sclerosis (SSc) is an autoimmune disease with fibrosis seen in multiple organs. Although not traditionally regarded as a disease of aging, SSc-associated fibrosis shares many of the hallmarks of aging seen in other age-related fibrotic disorders. Here, we review the current literature of the potential role of aging and age-related cellular processes in the development of SSc and fibrosis.
Recent findings: Accumulating evidence supports a role for immune dysregulation, epigenetic modifications, cellular senescence, mitochondrial dysregulation and impaired autophagy in fibrosis that occurs in aging and SSc.
Summary: Cellular alterations linked to aging may promote the development and/or progression of SSc-associated fibrosis.