IndraLab

Statements



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"In conclusion, USP38 promotes inflammatory AF induced by pressure overload."

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"Conversely, USP38 overexpression further increased susceptibility to AF by exacerbating atrial structural and electrical remodelling."

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"Overall, our study indicates that USP38 promotes pressure overload-induced AF through targeting NF-kappaB/NLRP3-mediated inflammatory responses."

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"Ubiquitin-specific protease 38 (USP38) was upregulated in the left atrium after aortic banding surgery.Cardiac-specific knockout of USP38 attenuated the atrial dilation and fibrosis and reduced the vulnerability of atrial fibrillation (AF) induced by pressure overload.Cardiac-specific overexpression of USP38 aggravated the atrial structural and electrical remodelling induced by pressure overload.Ubiquitin-specific protease 38 promoted atrial inflammation by interacting with and deubiquitinating nuclear factor-kappa B.Targeting USP38 may be an effective treatment for AF induced by pressure overload."

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"Ubiquitin-specific protease 38 (USP38) was upregulated in the left atrium after aortic banding surgery.Cardiac-specific knockout of USP38 attenuated the atrial dilation and fibrosis and reduced the vulnerability of atrial fibrillation (AF) induced by pressure overload.Cardiac-specific overexpression of USP38 aggravated the atrial structural and electrical remodelling induced by pressure overload.Ubiquitin-specific protease 38 promoted atrial inflammation by interacting with and deubiquitinating nuclear factor-kappa B.Targeting USP38 may be an effective treatment for AF induced by pressure overload."

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"It was found that overexpression of USP38 increased vulnerability to AF in diabetic mice."

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"USP38 overexpression increased susceptibility to AF, accompanied by aberrant expression of calcium-handling protein, heightened iron load and oxidation stress in diabetic mice."