Upregulation of p16INK4A promotes cellular senescence of bone marrow-derived mesenchymal stem cells from systemic lupus erythematosus patients

► MSCs from SLE patients showed characteristics of senescence. ► p16INK4A was increased in the MSCs from both untreated and treated SLE patients. ► Knockdown of p16INK4A reverse the senescent features of MSCs. ► p16INK4A promote MSCs senescence via suppression ERK1/2 signal pathway activation.