Peroxiredoxin 3 Inhibits Cardiac Fibrosis in Mice via NOX4-P38 Signalling. DOI

Xiaoqi Xiong,

Jun Li, Zhen Chen

и другие.

PubMed, Год журнала: 2023, Номер 25(6), С. 391 - 398

Опубликована: Июнь 28, 2023

Peroxiredoxin-3 (Prx-3) is widely acknowledged as an antioxidant that protects against mitochondrial reactive oxygen species. Nonetheless, its role in cardiac fibrosis has not been elucidated. We aim to explore the and mechanism of Prx-3 fibrosis.In this experimental study, mice received subcutaneous injections isoproterenol (ISO) for 14 consecutive days (10 mg/kg/d three days, followed by 5 11 days) establish a model. The were subsequently injected with adenovirus-Prx-3 (ad-Prx-3) enable overexpression. Echocardiography was used evaluate function. Mice heart fibroblasts isolated stimulated transforming growth factor β1 (TGFβ1) induce vitro. Cells also transfected ad-Prx-3 overexpression Prx-3.Echocardiographic diameters markers indicated could inhibit ISO-induced dysfunction fibrosis. Fibroblasts exhibited reduced activation, proliferation, collagen transcription. found expression NADPH oxidase 4 (NOX4) P38 levels. After treatment inhibitor, overexpression-induced anti-fibrosis effect mitigated.Prx-3 protect inhibiting NOX4-P38 pathway.

Язык: Английский

Peroxiredoxin 3 Inhibits Cardiac Fibrosis in Mice via NOX4-P38 Signalling. DOI

Xiaoqi Xiong,

Jun Li, Zhen Chen

и другие.

PubMed, Год журнала: 2023, Номер 25(6), С. 391 - 398

Опубликована: Июнь 28, 2023

Peroxiredoxin-3 (Prx-3) is widely acknowledged as an antioxidant that protects against mitochondrial reactive oxygen species. Nonetheless, its role in cardiac fibrosis has not been elucidated. We aim to explore the and mechanism of Prx-3 fibrosis.In this experimental study, mice received subcutaneous injections isoproterenol (ISO) for 14 consecutive days (10 mg/kg/d three days, followed by 5 11 days) establish a model. The were subsequently injected with adenovirus-Prx-3 (ad-Prx-3) enable overexpression. Echocardiography was used evaluate function. Mice heart fibroblasts isolated stimulated transforming growth factor β1 (TGFβ1) induce vitro. Cells also transfected ad-Prx-3 overexpression Prx-3.Echocardiographic diameters markers indicated could inhibit ISO-induced dysfunction fibrosis. Fibroblasts exhibited reduced activation, proliferation, collagen transcription. found expression NADPH oxidase 4 (NOX4) P38 levels. After treatment inhibitor, overexpression-induced anti-fibrosis effect mitigated.Prx-3 protect inhibiting NOX4-P38 pathway.

Язык: Английский

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