IndraLab

Statements

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"These abnormalities were markedly attenuated in USP38-CKO mice, suggesting that USP38 deficiency mitigates calcium mishandling."
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"Echocardiography revealed significant left atrial (LA) dilation in CKD mice (Fig. xref A, B and Supplementary Figure xref A), which was notably attenuated in USP38-CKO mice."
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"To elucidate the role of USP38 in modulating AF susceptibility in CKD, we generated cardiomyocyte-specific USP38 knockout (USP38-CKO) and overexpression (USP38-TG) mice (Supplementary Methods)."
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"Furthermore, USP38-CKO resulted in decreased STRAP expression in both atrial tissue and HL-1 cells (Fig. xref A-D), whereas USP38-TG led to increased STRAP expression in both models (Fig. xref E-H)."
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"To better elucidate the role of USP38 in regulation of HF-related VAs, we utilized the Cre-LoxP system to generate USP38-CKO mice, with their wild-type littermates referred to as the Flox-Sham group."
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"The absence of USP38 expression in the USP38-CKO mice were confirmed by Western blotting (Fig. S3A)."
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"After AB surgery, the Flox group exhibited a significant increase in QRS duration and QTc, However, these changes were attenuated in the USP38-CKO group following AB surgery (Fig.  xref A, B)."
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"Notably, USP38-CKO partially restored Cx40/Cx43 protein levels (Fig. xref A, B), whereas USP38-TG further suppressed their expression (Fig. xref C, D), thereby implicating USP38 in gap junction remodeling."
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"USP38-CKO attenuated atrial fibrosis and reduced collagen I/III and α-SMA expression, whereas USP38-TG exacerbated these effects."
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"Consistently, immunoblotting showed that USP38-CKO suppressed the CKD-induced upregulation of α-SMA and collagen I/III (Fig. xref E, F)."
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"The USP38-CKO group showed an improvement in the expression level of the above channel proteins (Fig.  xref A–F)."
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"The absence of USP38 protein in the heart was confirmed in USP38-CKO mice, whereas a marked overexpression was observed in USP38-TG hearts (Supplementary Figure xref )."
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"In USP38-CKO mice, these profibrotic mediators were significantly suppressed (Fig. xref A), whereas in USP38-TG mice, their activation was further enhanced (Fig. xref B), thereby linking USP38 to TGF-β–driven fibrogenesis."
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"However, both USP38-CKO and USP38-TG mice maintained CKD-induced AERP shortening without any significant improvement or exacerbation compared to the CKD-alone group (Fig. xref D, H)."
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"Specifically, we demonstrated that CKD mice exhibit a marked upregulation of USP38 in atrial tissue, and that cardiomyocyte-specific USP38 knockout (USP38-CKO) significantly attenuates atrial fibrosis and AF susceptibility."
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