ArticleExperimental and therapeutic medicine2019
Acetazolamide attenuates cardiac fibrosis induced by aortic constriction through inhibiting transforming growth factor-β1/Smad2 signaling pathway in mice.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 0 citations in OpenAlex.
- Aquaporin-1 upregulation is associated with scleral remodeling during myopia development in mice.American journal of translational research · 2026Article
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4 authors at 3 institutions in 1 country.
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Abstract
The effect and mechanism of acetazolamide on cardiac fibrosis induced by transverse aortic constriction (TAC) were investigated. C57BL/6 mice were subjected to TAC or sham operation and then were orally gavaged with acetazolamide (20 mg/kg/day). After 4 weeks of operation, cardiac function was detected by echocardiography. Interstitial fibrosis was stained with Masson's trichrome. The expression of α-smooth muscle actin (α-SMA), collagen I, transforming growth factor-β1 (TGF-β1) and Smad2 were measured by western blotting. The TAC mice displayed significant cardiac dysfunction and fibrosis. The expression of α-SMA, collagen I, TGF-β1 and p-Smad2 in the TAC group was higher than those in the sham group. By contrast, acetazolamide administration inhibited interstitial fibrosis, as well as improved cardiac dysfunction induced by TAC. Acetazolamide also reduced the expression of α-SMA, collagen I, TGF-β1 and p-Smad2 in the TAC mice. Acetazolamide was able to attenuate cardiac fibrosis and improve cardiac dysfunction. The molecular mechanism involved in the anti-fibrotic effect of acetazolamide possibly was through inhibiting TGF-β1/Smad2 signaling pathway.
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