Sodium Selenite Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension by Upregulating GPX3 and Ameliorating Vascular Remodeling.

Selenium deficiency is implicated in pulmonary arterial hypertension (PAH). This study investigated the effects of sodium selenite (SSE) on PAH and its underlying mechanisms. In a monocrotaline-induced PAH rat model, SSE treatment significantly improved right ventricular systolic pressure (RVSP), me...

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Publicado en:Physiological Research Vol. 75; no. 2; pp. 325 - 336
Autores principales: LIU, Zihua, LIU, Xue, MPRAH, Richard, SUN, Hong, ADU-AMANKWAAH, Joseph, PAN, Xiuhua, CHENG, Shouquan, XIE, Bing, WANG, Cheng, QIAO, Weili
Formato: Journal Article
Publicado: Institute of Physiology, Academy of Sciences of the Czech Republic Apr2026
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Apr2026
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      pub: Institute of Physiology, Academy of Sciences of the Czech Republic
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        10.33549/physiolres.935734
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        atl: Sodium Selenite Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension by Upregulating GPX3 and Ameliorating Vascular Remodeling.
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        au:
          LIU, Zihua
          LIU, Xue
          MPRAH, Richard
          SUN, Hong
          ADU-AMANKWAAH, Joseph
          PAN, Xiuhua
          CHENG, Shouquan
          XIE, Bing
          WANG, Cheng
          QIAO, Weili
        affil: Department of Physiology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
      sug:
      ab: Selenium deficiency is implicated in pulmonary arterial hypertension (PAH). This study investigated the effects of sodium selenite (SSE) on PAH and its underlying mechanisms. In a monocrotaline-induced PAH rat model, SSE treatment significantly improved right ventricular systolic pressure (RVSP), mean pulmonary arterial pressure (mPAP), and vascular remodeling. It reduced collagen deposition and partially restored the expression of Collagen 1 and SM22α. SSE upregulated glutathione peroxidase 3 (GPX3) expression and attenuated oxidative stress, as evidenced by enhanced SOD activity and decreased MDA levels. In vitro, SSE inhibited H₂O₂ and angiotensin II-induced proliferation, oxidative stress, and phenotypic switching in pulmonary artery smooth muscle cells (PASMCs), while upregulating GPX3 at both mRNA and protein levels. These findings demonstrate that SSE alleviates PAH by enhancing GPX3-mediated antioxidant defense and suppressing vascular remodeling, supporting its potential as a therapeutic strategy for PAH.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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