The roles of orphan nuclear receptor 4 group A1 and A2 in fibrosis

Fibrosis is not a disease but rather an outcome of the pathological tissue repair response. Many myofibroblasts are activated which lead to the excessive accumulation of extracellular matrix components such as collagen and fibronectin with fibrosis. A variety of organs, including kidney, liver, lung, heart and skin, can undergo fibrosis under the stimulation of exogenous or endogenous pathogenic factors. The orphan nuclear receptor 4 group A1 (NR4A1) and nuclear receptor 4 group A2（NR4A2）are belong to the nuclear receptor subfamily and inhibit the occurrence and development of fibrosis. NR4A1 is an inhibitory factor of TGF-β signaling transduction. Overexpression of NR4A1 in fibroblasts can reduce TGF-β induced collagen deposition and fibrosis related gene expression. Here, we summarize the current research progress on the NR4A1/2 and fibrosis, providing reference for the treatment of fibrosis.