Peroxiredoxin 3 Inhibits Cardiac Fibrosis in Mice via NOX4-P38 Signalling
نویسندگان
1 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
2 Department of Emergency, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan City, Hubei Province, P.R. China
3 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
4 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
5 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
6 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
7 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
8 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
9 Department of Emergency, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan City, Hubei Province, P.R. China
10 Department of Cardiology, Liuzhou Municipal Liutie Central Hospital, Liuzhou City, Guang Xi Province, P.R. China
doi
10.22074/cellj.2023.557603.1082چکیده
Objective: Peroxiredoxin-3 (Prx-3) is widely acknowledged as an antioxidant that protects against mitochondrialreactive oxygen species. Nonetheless, its role in cardiac fibrosis has not been elucidated. We aim to explore the roleand mechanism of Prx-3 in cardiac fibrosis.Materials and Methods: In this experimental study, mice received subcutaneous injections of isoproterenol (ISO) for 14consecutive days (10 mg/kg/d for three days, followed by 5 mg/kg/d for 11 days) to establish a cardiac fibrosis model. Themice were subsequently injected with adenovirus-Prx-3 (ad-Prx-3) to enable Prx-3 overexpression. Echocardiographywas used to evaluate cardiac function. Mice heart fibroblasts were isolated and stimulated with transforming growthfactor β1 (TGFβ1) to induce fibrosis in vitro. Cells were also transfected with ad-Prx-3 for overexpression of Prx-3.Results: Echocardiographic diameters and fibrosis markers indicated that Prx-3 could inhibit ISO-induced cardiacdysfunction and fibrosis. Fibroblasts with Prx-3 overexpression exhibited reduced activation, proliferation, and collagentranscription. We found that Prx-3 reduced the expression of NADPH oxidase 4 (NOX4) and reduced P38 levels. Aftertreatment with a P38 inhibitor, the Prx-3 overexpression-induced anti-fibrosis effect was mitigated.Conclusion: Prx-3 could protect against ISO-induced cardiac fibrosis by inhibiting the NOX4-P38 pathway.
