Publications by authors named "Yuetao Xie"

5 Publications

  • Page 1 of 1

Thrombus aspiration during primary percutaneous coronary intervention improved outcome in patients with STEMI and a large thrombus burden.

J Int Med Res 2021 May;49(5):3000605211012611

Department of Cardiology Center, Hebei General Hospital, Shijiazhuang, No.348 West Peace Road, Xinhua District, Shijiazhuang, Hebei Province, People's Republic of China.

Background: The benefit of thrombus aspiration (TA) during primary percutaneous coronary intervention (PPCI) to patients with ST-segment elevation myocardial infarction (STEMI) remains controversial. This study aimed to assess TA's impact on the outcome and prognosis for patients with STEMI and a large thrombus burden during PPCI.

Methods: This retrospective study evaluated consecutive patients with STEMI and a large thrombus burden (thrombolysis in myocardial infraction [TIMI] thrombus grade ≥4) who underwent conventional PPCI (n = 126) or PPCI + TA (n = 208) between February 2017 and January 2019. The procedure outcome and clinical prognosis were compared.

Results: Postprocedural vessel diameter was larger, and corrected TIMI frame count (cTFC) was lower in the PPCI + TA compared with the PPCI group. The proportion of postprocedural TIMI 3 flow was 83.3% in the PPC group and 94.2% in the PPCI+TA group. During the 12-month follow-up, no significant differences existed in the incidence of cardiac death, reinfarction, stent thrombosis, target vessel revascularization, or stroke.

Conclusion: Application of TA in patients with STEMI and a large thrombus burden during PPCI may improve the procedural outcome, but it showed no benefit on the clinical prognosis in the 12-month follow-up. Longer follow-up studies are needed to confirm TA's clinical implications in patients with STEMI.
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http://dx.doi.org/10.1177/03000605211012611DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8113933PMC
May 2021

miR-362-3p Targets Orosomucoid 1 to Promote Cell Proliferation, Restrain Cell Apoptosis and Thereby Mitigate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury.

Cardiovasc Toxicol 2021 May 18;21(5):387-398. Epub 2021 Jan 18.

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

This study aimed to investigate the mechanism of how miR-362-3p/orosomucoid 1 (ORM1) involved in hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. Based on data obtained from Gene Expression Omnibus (GEO) database, we revealed that ORM1 was highly expressed and positively correlated with the expression of inflammatory factors (MAPK1, MAPK3, IL1B and CASP9). miR-362-3p was identified as an upstream regulatory miRNA of ORM1 and negatively modulated the mRNA and protein expression levels of ORM1 in H/R-injured cardiomyocytes. Moreover, we found that miR-362-3p was downregulated in cardiomyocytes injured by H/R. The promoting influence of miR-362-3p mimic on the proliferation and the inhibitory effect of miR-362-3p mimic on the apoptosis of H/R-stimulated cardiomyocytes were eliminated by overexpression of ORM1. Furthermore, miR-362-3p affected the expression of MAPK1, MAPK3, IL1B and CASP9 in H/R-injured cardiomyocytes through targeting ORM1. Our outcomes illustrated that miR-362-3p exhibited a protective influence on H/R-induced cardiomyocytes through targeting ORM1.
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http://dx.doi.org/10.1007/s12012-020-09631-0DOI Listing
May 2021

Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury.

Mediators Inflamm 2020 24;2020:8869511. Epub 2020 Nov 24.

Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.

Objective: Renal ischemia/reperfusion injury (RI/RI) is the main cause of acute kidney injury. Total glucosides of paeony (TGP) are a traditional Chinese medicine. This study was aimed at exploring the role of TGP in RI/RI and its underlying mechanism of action.

Methods: Rat RI/RI models were constructed by surgical operation. Serum creatinine (Scr) and blood urea nitrogen (BUN) were used to evaluate renal function. The levels of proinflammatory cytokines were detected by ELISA. RI/RI was simulated by hypoxia/reoxygenation (H/R) treatment in renal cells . The lncRNA XIST (XIST) expression was analyzed by qRT-PCR. Then, the viability and apoptosis of renal cells were detected by MTT and flow cytometry assay. Additionally, dual-luciferase reporter assay was used to determine the interactions among XIST, microRNA-124-3p (miR-124-3p), and ITGB1.

Results: TGP improved renal function and inhibited inflammatory responses after RI/RI. XIST expression was highly expressed in rat RI/RI models and H/R-treated renal cells, whereas treatment with TGP downregulated the XIST expression. Additionally, TGP increased viability and attenuated apoptosis and inflammation of H/R-treated renal cells via inhibiting XIST. Moreover, XIST was competitively bound to miR-124-3p, and ITGB1 was a target of miR-124-3p. miR-124-3p overexpression or ITGB1 inhibition rescued the reduction effect on viability and mitigated the promoting effects on cell apoptosis and inflammation caused by XIST overexpression in H/R-treated renal cells.

Conclusions: , TGP attenuated renal dysfunction and inflammation in RI/RI rats. , TGP inhibited XIST expression to modulate the miR-124-3p/ITGB1 axis, alleviating the apoptosis and inflammation of H/R-treated renal cells.
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http://dx.doi.org/10.1155/2020/8869511DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7710434PMC
November 2020

CAR T-cell therapy for triple-negative breast cancer: Where we are.

Cancer Lett 2020 10 12;491:121-131. Epub 2020 Aug 12.

Department of Anesthesiology, Shenzhen Children's Hospital, Shenzhen, Guangdong, 518038, China. Electronic address:

Triple-negative breast cancer (TNBC) is the most complex and challenging breast cancer subtype to treat, and chemotherapy remains the standard of care. Clinically, TNBC has a relatively high rate of recurrence and poor prognosis, which leads to a significant effort to discover novel strategies to treat patients with these tumors. Currently, chimeric antigen receptor (CAR) T cell-based immunotherapy redirects the patient's immune system directly to recognize and eradicate tumor-associated antigens (TAAs) expressing tumor cells being explored as a treatment for TNBC. A steadily increasing research in CAR T-cell therapy targeting different TAAs in TNBC has reported. In this review, we introduce the CAR technology and summarize the potential TAAs, available CARs, the antitumor activity, and the related toxicity of CARs currently under investigation for TNBC. We also highlight the potential strategies to prevent/reduce potential "on target, off tumor" toxicity induced by CAR T-cell therapy. This review will help to explore proper targets to expand further the CAR T-cell therapy for TNBCs in the clinic.
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http://dx.doi.org/10.1016/j.canlet.2020.07.044DOI Listing
October 2020

Inhibition of SETD7 protects cardiomyocytes against hypoxia/reoxygenation-induced injury through regulating Keap1/Nrf2 signaling.

Biomed Pharmacother 2018 Oct 11;106:842-849. Epub 2018 Jul 11.

Department of Cardiology, Hebei General Hospital, No.348 West Heping Road, Shijiazhuang, Hebei 050051, China. Electronic address:

The protein SET domain-containing lysine methyltransferase 7 (SETD7) has recently been shown to regulate apoptosis in various cells. However, the role of SETD7 on cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury remains unclear. This study aimed to investigate the potential role of SETD7 in hypoxia/reoxygenation (H/R)-induced apoptosis of rat cardiomyocytes and reveal the underlying mechanism. Our results demonstrated that SETD7 expression was significantly up-regulated in cardiomyocytes in response to H/R injury. The inhibition of SETD7 by siRNA-mediated gene silencing significantly suppressed H/R-induced apoptosis and decreased the production of reactive oxygen species (ROS). The overexpression of SETD7 markedly enhanced H/R-induced apoptosis and ROS production. Moreover, the knockdown of SETD7 reduced the expression of Keap1 and promoted the expression of Nrf2. In addition, the knockdown of SETD7 increased the activity of antioxidant response element and promoted the expression of heme oxygenase-1 and NADPH-quinone oxidoreductase 1. However, the knockdown of Nrf2 partially abrogated the SETD7 inhibition-mediated protective effect against H/R injury. Taken together, these results indicate that the inhibition of SETD7 attenuates H/R-induced injury of cardiomyocytes via the down-regulation of Keap1 and promotion of the Nrf2-mediated anti-oxidation signaling pathway.
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http://dx.doi.org/10.1016/j.biopha.2018.07.007DOI Listing
October 2018