JULING FENG^1,3, HAODONG CHEN¹, YANGBO LIU¹, QIDI AI¹, YANTAO YANG¹, LEI ZHAO⁴, SHIFENG CHU^2,#,*, NAIHONG CHEN^1,2,#,*

BIOCELL, Vol.48, No.6, pp. 981-990, 2024, DOI:10.32604/biocell.2024.050011 - 10 June 2024

Abstract Introduction: Chemokine-like factor 1 (CKLF1) is a chemokine that is overexpressed in several diseases. Our previous findings revealed a significant increase in CKLF1 expression in the ischemic brain, suggesting its potential as a therapeutic target for ischemic stroke. Methods: In this study, we examined the expression dynamics of CKLF1 in both in vivo and in vitro models of ischemic cardiac injury. Myocardial infarction (MI) was induced in vivo by ligation of the left anterior descending artery (LAD) of the rat heart. The levels of CKLF1, Creatine Kinase MB Isoenzyme (CK-MB), and Lactate dehydrogenase (LDH) in the serum were… More > Graphic Abstract

FEI KONG¹, QIYUAN TIAN², BINGLIN KUANG³, LILI SHANG⁴, XIAOXIAO ZHANG⁵, DONGYANG LI⁵, YING KONG^6,*

BIOCELL, Vol.48, No.4, pp. 665-675, 2024, DOI:10.32604/biocell.2024.046342 - 09 April 2024

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,… More > Graphic Abstract

QI SONG¹, JUN ZHANG¹, QIANG ZHANG¹, JING LIU¹, KE LV¹, JIALU YAO^1,2,3,*, YAFENG ZHOU^2,3,*

BIOCELL, Vol.44, No.4, pp. 623-629, 2020, DOI:10.32604/biocell.2020.012645 - 24 December 2020

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 More >

Domenico Sirico¹, Biagio Castaldi^1,*, Giuseppe Tarantini², Giovanni Di Salvo¹

Congenital Heart Disease, Vol.15, No.6, pp. 441-445, 2020, DOI:10.32604/CHD.2020.012863 - 02 November 2020

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 More >

XINGXING ZHU^1,2, TIANFENG HUA^1,2, MINGFEI WU³, JIATIAN WU^1,2, JIANCHAO HONG^1,2, MIN YANG^1,2,*

BIOCELL, Vol.44, No.3, pp. 431-441, 2020, DOI:10.32604/biocell.2020.010323 - 22 September 2020

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 More >

Ian S. Rogers^1,2, 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 >

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 More >

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, More >