Role of USP13 in physiology and diseases

Abstract

Ubiquitin specific protease (USP)-13 is a deubiquitinase that removes ubiquitin from substrates to prevent protein degradation by the proteasome. Currently, the roles of USP13 in physiology and pathology have been reported. In physiology, USP13 is highly associated with cell cycle regulation, DNA damage repair, myoblast differentiation, quality control of the endoplasmic reticulum, and autophagy. In pathology, it has been reported that USP13 is important in the pathogenesis of infection, inflammation, idiopathic pulmonary fibrosis (IPF), neurodegenerative diseases, and cancers. This mini-review summarizes the most recent advances in USP13 studies involving its pathophysiological roles in different conditions and provides new insights into the prevention and treatment of relevant diseases, as well as further research on USP13.

LncRNA FRMD6‐AS1/miR‐491‐5p/USP13 pathway attenuated ferroptosis and contributed to liver fibrosis

“…Knockdown of USP13 accelerated lung fibroblasts phenotypic changes and contributed to pulmonary fibrosis. 29,30 USP13 loss facilitated susceptibility to bleomycin-induced lung fibrosis in vivo model. 50 USP13 expression was up-regulated in lung fibroblasts, and USP13 deficient decreased ECM expression (collagen, SMA, and fibronectin).…”

“…Several studies have shown that USP13 exerted important functions in modulating lung fibrosis and ECM deposition. Knockdown of USP13 accelerated lung fibroblasts phenotypic changes and contributed to pulmonary fibrosis 29,30 . USP13 loss facilitated susceptibility to bleomycin‐induced lung fibrosis in vivo model 50 .…”

“…Ubiquitin‐specific protease 13 (USP13) is a vital factor in innate immune responses, energy metabolism, autophagy, DNA damage response in different diseases, and can act as a tumor promoter in cancers 28 . Reports have found that USP13 was critical in the pathogenetic mechanism of pulmonary fibrosis, and knockdown of USP13 promoted lung fibroblasts phenotypic changes and contributes to pulmonary fibrosis 29,30 . Besides, USP13 overexpression reversed the repression of Spautin‐1‐induced autophagy and ferroptosis in cerebral ischemia–reperfusion injury 31 .…”

“…28 Reports have found that USP13 was critical in the pathogenetic mechanism of pulmonary fibrosis, and knockdown of USP13 promoted lung fibroblasts phenotypic changes and contributes to pulmonary fibrosis. 29,30 Besides, USP13 overexpression reversed the repression of Spautin-1-induced autophagy and ferroptosis in cerebral ischemia-reperfusion injury. 31 In addition, USP13 was elevated in hepatocellular carcinoma tissues and cells, 32 however, the role of USP13 in liver fibrosis is not clear.…”

Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression

“…USP13 has been known to participate in the pathogenesis of infection, cancers, inflammation and neurodegenerative diseases (115). For example, USP13 inhibited lung inflammation via stabilization of the anti-inflammatory receptor IL-1R8/single immunoglobin interleukin-1-related receptor (Sigirr) (116).…”