Trastuzumab-induced human cardiomyocyte damage through the Notch2/JAK2/STAT3 pathway

Su, Zhenbo; Liu, Siyao; Zou, Yinggang; Shan, Liang; Yu, Miao; Xie, Shishun; Li, X Q; Jin, Ying

doi:10.1016/j.clinsp.2023.100268

Cited by 2 publications

(1 citation statement)

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“…We constructed gene modules through unsupervised clustering and selected the modules most relevant to HCM. Notably, key modules included genes such as RHOA [ 22 ] and JAK2 [ 23 ], which have been previously reported to be associated with HCM. Previous studies have confirmed that transcriptional regulation of JAK2 in verified cases of HCM is correlated with increased global ventriculus sinister and cardiomyocyte nuclear JAK2 expression, as well as the activation of its downstream canonical target, STAT3 [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analyses and Experimental Validation Identified Immune-Related lncRNA–mRNA Pair MIR210HG–BPIFC Regulating the Progression of Hypertrophic Cardiomyopathy

Zhang,

Zhao,

Jin

et al. 2024

IJMS

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Hypertrophic cardiomyopathy (HCM) is a disease in which the myocardium of the heart becomes asymmetrically thickened, malformed, disordered, and loses its normal structure and function. Recent studies have demonstrated the significant involvement of inflammatory responses in HCM. However, the precise role of immune-related long non-coding RNAs (lncRNAs) in the pathogenesis of HCM remains unclear. In this study, we performed a comprehensive analysis of immune-related lncRNAs in HCM. First, transcriptomic RNA-Seq data from both HCM patients and healthy individuals (GSE180313) were reanalyzed thoroughly. Key HCM-related modules were identified using weighted gene co-expression network analysis (WGCNA). A screening for immune-related lncRNAs was conducted within the key modules using immune-related mRNA co-expression analysis. Based on lncRNA–mRNA pairs that exhibit shared regulatory microRNAs (miRNAs), we constructed a competing endogenous RNA (ceRNA) network, comprising 9 lncRNAs and 17 mRNAs that were significantly correlated. Among the 26 lncRNA–mRNA pairs, only the MIR210HG–BPIFC pair was verified by another HCM dataset (GSE130036) and the isoprenaline (ISO)-induced HCM cell model. Furthermore, knockdown of MIR210HG increased the regulatory miRNAs and decreased the mRNA expression of BPIFC correspondingly in AC16 cells. Additionally, the analysis of immune cell infiltration indicated that the MIR210HG–BPIFC pair was potentially involved in the infiltration of naïve CD4+ T cells and CD8+ T cells. Together, our findings indicate that the decreased expression of the lncRNA–mRNA pair MIR210HG–BPIFC was significantly correlated with the pathogenesis of the disease and may be involved in the immune cell infiltration in the mechanism of HCM.

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Section: Discussionmentioning

confidence: 99%