SFRP5 serves a beneficial role in arterial aging by inhibiting the proliferation, migration and inflammation of smooth muscle cells.

Secreted frizzled-related protein 5 (SFRP5) is one of the anti-inflammatory adipokines secreted from white adipose tissue. However, little is known about the effect of SFRP5 on the cardiovascular system. The aim of the present study was to determine the effect of SFRP5 on smooth muscle cell (SMC) proliferation, migration and inflammation. The plasma levels of SFRP5 were evaluated in a cohort‑based elderly population using ELISA, and the expression of SFRP5 in Sprague‑Dawley rat aortas was detected using immunohistochemistry. SMC proliferation and migration were evaluated in vitro using 5‑ethynyl‑2'‑deoxyuridine cell proliferation and wound‑healing assays, respectively, while reactive oxygen species (ROS) production and cell signaling were assessed using a 2',7'‑dichlorodihydrofluorescein diacetate assay and immunoblotting, respectively. The results revealed that plasma levels of SFRP5 were positively correlated with age in the elderly Chinese cohort. Similarly, aorta SFRP5 expression was significantly higher in 15‑month‑old rats compared with 6‑month‑old rats. In vitro, SFRP5 significantly inhibited rat aortic SMC proliferation and migration that were induced by platelet‑derived growth factor (PDGF)‑BB, as well as inhibiting ROS generation. Compared with the effect of PDGF‑BB on SMCs, SFRP5 at 100 and 200 ng/ml significantly decreased SMC proliferation by 31.5 and 34.8%, respectively (P<0.05). SFRP5 at 100 and 200 ng/ml also inhibited the migration of SMCs by 24.9 and 28.4%, respectively, when compared with the effects of PDGF‑BB. SFRP5 attenuated the PDGF‑BB‑induced expression of β‑catenin and proliferating cell nuclear antigen, while p38 phosphorylation was significantly attenuated. Together, the present results suggested that SFRP5 may inhibit SMC proliferation, migration and inflammation by suppressing the Wnt/β‑catenin and p38/mitogen‑activated protein kinase signaling pathways.