Furthermore, HMGB1 in the inflammatory BM microenvironment can promote the senescence of MSCs via the TLR2/4 and NF-κB signaling pathways, and inhibition of HMGB1 by ethyl pyruvate (EP) can improve lupus nephritis and reverse senescence-associated secretory phenotype (SASP) development [93, 94]. This evidence concerns the gene HMGB1 and lupus nephritis.