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.