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  • Open Access

    ARTICLE

    Inhibition of SLC26A4 regulated by electroacupuncture suppresses the progression of myocardial ischemia-reperfusion injury

    FEI KONG1, QIYUAN TIAN2, BINGLIN KUANG3, LILI SHANG4, XIAOXIAO ZHANG5, DONGYANG LI5, YING KONG6,*

    BIOCELL, Vol.48, No.4, pp. 665-675, 2024, DOI:10.32604/biocell.2024.046342

    Abstract Introduction: Myocardial ischemia-reperfusion (IR) injury has received widespread attention due to its damaging effects. Electroacupuncture (EA) pretreatment has preventive effects on myocardial IR injury. SLC26A4 is a Na+ independent anion reverse transporter and has not been reported in myocardial IR injury. Objectives: To find potential genes that may be regulated by EA and explore the role of this gene in myocardial IR injury. Methods: RNA sequencing and bioinformatics analysis were performed to obtain the differentially expressed genes in the myocardial tissue of IR rats with EA pretreatment. Myocardial infarction size was detected by TTC staining. Serum CK, creatinine kinase-myocardial band,… More > Graphic Abstract

    Inhibition of SLC26A4 regulated by electroacupuncture suppresses the progression of myocardial ischemia-reperfusion injury

  • Open Access

    ARTICLE

    Exosomes derived from circBCRC-3-knockdown mesenchymal stem cells promoted macrophage polarization

    QI SONG1, JUN ZHANG1, QIANG ZHANG1, JING LIU1, KE LV1, JIALU YAO1,2,3,*, YAFENG ZHOU2,3,*

    BIOCELL, Vol.44, No.4, pp. 623-629, 2020, DOI:10.32604/biocell.2020.012645

    Abstract Macrophages play an essential role in the myocardial ischemia-reperfusion injury (MIRI), and the macrophage shifting from M1 to M2 phenotypes might be a potential strategy for the treatment of MIRI. It has been reported that miR-182 plays an important role in MSC-Exo-associated macrophage polarization. As circBCRC-3 is a newly discovered circle RNA that worked as a sponge of miR-182, this research aimed to find if circBCRC-3 plays a role in MSC-Exo-associated macrophage polarization. Firstly, circBCRC-3 was identified by divergent primers in mesenchymal stem cells (MSCs). Secondly, the exosome of MSCs was isolated and identified by transmission electron microscopy (TEM), nanoparticle-tracking… More >

  • Open Access

    CASE REPORT

    FFR-Guided PCI in a 17-Year-Old Patient after Arterial Switch Operation for D-Transposition of the Great Arteries

    Domenico Sirico1, Biagio Castaldi1,*, Giuseppe Tarantini2, Giovanni Di Salvo1

    Congenital Heart Disease, Vol.15, No.6, pp. 441-445, 2020, DOI:10.32604/CHD.2020.012863

    Abstract Asymptomatic coronary artery obstruction represents a significant diagnostic challenge in patients with Dextro-Transposition of the Great Arteries and history of Arterial Switch Operation. We report the case of a 17-year-old boy with anomalous origin of left circumflex artery from the right coronary artery, who underwent neonatal arterial switch operation and developed silent myocardial ischemia under stress on myocardial scintigraphy. Despite coronary angiogram and intravascular ultrasound showed only intermediate stenosis of the right coronary artery ostium, the physiological analysis, through the employment of pressure wire, demonstrated a severe reduction of coronary fractional flow reserve after pharmacologically induced hyperemia. Thus, the patient… More >

  • Open Access

    ARTICLE

    Cardioprotective effect of ivabradine via the AMPK/SIRT1/PGC-1α signaling pathway in myocardial ischemia/reperfusion injury induced in H9c2 cell

    XINGXING ZHU1,2, TIANFENG HUA1,2, MINGFEI WU3, JIATIAN WU1,2, JIANCHAO HONG1,2, MIN YANG1,2,*

    BIOCELL, Vol.44, No.3, pp. 431-441, 2020, DOI:10.32604/biocell.2020.010323

    Abstract Post-resuscitation myocardial dysfunction (PRMD) is the most severe myocardial ischemia-reperfusion injury (MIRI) and is characterized by difficult treatment and poor prognosis. Research has shown the protective effects of the rational use of ivabradine (IVA) against PRMD; however, the molecular mechanisms of IVA remain unknown. In this study, an ischemia-reperfusion injury (IRI) model was established using hypoxic chambers. The results demonstrated that pretreatment with IVA reduced IRI-induced cytotoxicity and apoptosis. IVA attenuated mitochondrial damage, eliminated excess reactive oxygen species (ROS), suppressed IRI-induced ATP and NAD+ , and increased the AMP/ATP ratio. We further found that IVA increased the mRNA levels of… More >

  • Open Access

    ARTICLE

    Myocardial bridges: Overview of diagnosis and management

    Ian S. Rogers1,2, Jennifer A. Tremmel1, Ingela Schnittger1

    Congenital Heart Disease, Vol.12, No.5, pp. 619-623, 2017, DOI:10.1111/chd.12499

    Abstract A myocardial bridge is a segment of a coronary artery that travels into the myocardium instead of the normal epicardial course. Although it is general perception that myocardial bridges are normal variants, patients with myocardial bridges can present with symptoms, such as exertional chest pain, that cannot be explained by a secondary etiology. Such patients may benefit from individualized medical/ surgical therapy. This article describes the prevalence, clinical presentation, classification, evaluation, and management of children and adults with symptomatic myocardial bridges. More >

  • Open Access

    ARTICLE

    Kawasaki disease: State of the art

    Jane W. Newburger

    Congenital Heart Disease, Vol.12, No.5, pp. 633-635, 2017, DOI:10.1111/chd.12498

    Abstract Kawasaki disease is an acute febrile arteritis of childhood that can result in coronary artery aneurysms if untreated in the first 10 and ideally 7 days of illness. Kawasaki disease begins as a necrotizing arteritis with neutrophilic infiltrate, followed by subacute/chronic changes and luminal myofibroblastic proliferation that can cause coronary artery stenosis. Manifestations include the presence of ≥5 days of fever, together with clinical criteria of extremity changes, rash, conjunctivitis, oral changes, and unilateral cervical lymphadenopathy. Echocardiography should be performed at the time of diagnosis, then 1–2 weeks and 4–6 weeks later, with more frequent studies in individuals with coronary… More >

  • Open Access

    REVIEW

    Cardioprotective Mechanisms Activated in Response to Myocardial Ischemia

    Shu Q. Liu∗,†, Brandon J. Tefft*, Di Zhang*, Derek Roberts*, Daniel J. Schuster*, Allison Wu*

    Molecular & Cellular Biomechanics, Vol.8, No.4, pp. 319-338, 2011, DOI:10.3970/mcb.2011.008.319

    Abstract Myocardial ischemia, a disorder causing myocardial infarction and malfunction, can activate various adaptive mechanisms that protect cardiomyocytes from ischemic injury. During the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which promote myocardial survival by activating the G protein signaling pathways. During a later phase about several days, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF, HGF, and SDF-1, in the injured myocardium, contributing to cardioprotection. In addition to the injured heart, the liver participates in cardioprotection. In response to myocardial ischemia, the liver upregulates and releases… More >

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