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Cardiomyocytes - DOAJ

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Last Updated: 10 January 2023

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Brugada Syndrome: Different Experimental Models and the Role of Human Cardiomyocytes From Induced Pluripotent Stem Cells

Brugada syndrome is an inherited and rare cardiac arrhythmogenic disorder that is associated with an elevated risk of ventricular fibrillation and sudden cardiac death. Only a few BrS studies have used humanu2010-induced pluripotent stem cellu2013derived cardiomyocytes, the majority of which have concentrated on genotype correlations and drug screening. This paper sought to compare different BrS models in order to gain a better understanding of the roles of human-u2010-induced pluripotent stem cell cellu2013derived cardiomyocytes in recent BrS research and personalized medicine at a later stage.

Source link: https://doi.org/10.1161/JAHA.121.024410


Quantitative proteomics analysis revealed the potential role of lncRNA Ftx in cardiomyocytes

Abstract Objectives: The aim of this research is to decode the proteomic signature of cardiomyocytes in reaction to lncRNA Ftx knockdown and overexpression by proteomic analysis, as well as the biological role of lncRNA Ftx in cardiomyocytes. Methods: The lncRNA Ftx expression in cardiomyocytes cultured in vitro was changed, and cardiovascular hemoglobule changes were quantitatively determined by liquid chromatography-mass spectrometry. In the lncRNA Ftx knockdown group, a 1. 5-fold change threshold, 32 upregulated proteins, and 49 downregulated proteins are all found, while 49 downregulated proteins and 49 downregulated proteins are identified, while 67 up-regulated proteins and 54 down-regulated proteins are identified. The lncRNA Ftx is involved in controlling cardiomyocyte apoptosis and ferroptosis as well as increasing cellular energy metabolism, according to a functional clustering analysis of differential genes. Conclusion This research shows that lncRNA Ftx plays a crucial role in cardiomyocytes and may be involved in the occurrence and development of various myocardial disorders.

Source link: https://doi.org/10.1186/s12953-022-00201-6


Ticagrelor reduces doxorubicin-induced pyroptosis of rat cardiomyocytes by targeting GSK-3β/caspase-1

The role of ticagrelor in pyroptosis has been shown to contribute to the pathological process of pyroptosis, but it is unclear if it is related to the potential role of ticagrelor. In this research, we investigated the effects of ticagrelor on cardiomyocytes' Dox-induced pyroptosis. Rats were treated with ticagrelor 1 h before intravenous injection of Dox, one every 3 days, six times in total. Ticagrelor was shown to dramatically improve cardiac function by blocking GSK-3-1/GSDMD induction by inhibiting GSK-3u03b2/caspase-1/GSDMD activation. Using rat cardiac myocytes and rat embryonic cardiac-derived H9c2 cells, In vitro experiments were carried out. We found that ticagrelor inhibited the proliferation of Akt caused by Dox in the heart tissue as well as in Dox-induced RCMs/H9c2 cells. The inhibitory effect of ticagrelor on Dox-induced caspase-1/GSDMD expression in H9c2 cells was diminished when GSK-3b2 expression was absent in H9c2 cells. These results revealed that ticagrelor reduced Dox-induced pyroptosis in rat cardiomyocytes by affecting GSK-3-paspase-1.

Source link: https://doi.org/10.3389/fcvm.2022.1090601


Canagliflozin Attenuates Lipotoxicity in Cardiomyocytes by Inhibiting Inflammation and Ferroptosis through Activating AMPK Pathway

Diabetic cardiomyopathy is a myocardial disorder that is unrelated to other cardiovascular disorders, such as coronary heart disease, hypertension, etc. Lipotoxicity is closely related to DCM and is closely related to DCM. In this research, we investigated the origins of lipid metabolism imbalance in DCM in HL-1 cells. We discovered that canagliflozin significantly reduced the expression of inflammatory factors cyclooxygenase-2 and inducible nitric oxide synthase through bioinformatics and Western blotting experiments. By determining intracellular Fe 2+ content, ferroptosis in cardiomyocytes, reduced glutathione, and mitochondrial membrane potential, we established the presence of ferroptosis in cardiomyocytes.

Source link: https://doi.org/10.3390/ijms24010858


Brain Natriuretic Peptide Protects Cardiomyocytes from Apoptosis and Stimulates Their Cell Cycle Re-Entry in Mouse Infarcted Hearts

After infarction, brain natriuretic Peptide supplementation improves heart function and reduces heart remodeling. In vitro BNP-treated adult CMs and in CMs isolated from BNP-treated hearts, the signaling pathway triggered by BNP treatment was found. According to Troponin T plasma concentration, it was significantly reduced 1 and 3 days after infarction in BNP-treated mice, resulting in less CM deaths. CMs isolated from saline-treated hearts have higher mRNAs coding for hif1 alpha and for the various cyclins than CMs isolated from saline-treated hearts. Adult CMs in vivo are mediated by NPR-A binding and activation of the ERK MAP kinase pathway. BNP and all therapies aimed at raising BNP's bioavailability as new cardioprotective goals, according to Altogether's findings, as BNP therapy results in an elevated number of CMs in neonatal, adult unmanipulated, and infarcted hearts.

Source link: https://doi.org/10.3390/cells12010007


Effects of sevoflurane and its metabolite hexafluoroisopropanol on hypoxia/reoxygenation-induced injury and mitochondrial bioenergetics in murine cardiomyocytes

We wanted to find out how sevoflurane and its primary metabolite hexafluopropanol may have an effect on necrosis, apoptosis, and reactive oxygen species formation in cardiomyocytes following hypoxia/reoxygenation injury. Methods: Murine cardiomyocytes were exposed to hypoxia, followed by oxidation in the presence or absence of sevoflurane 2. 2% or HFIP 4 mM. Result: Hypoxia/reoxygenation triggered cell death by 44%. The increase in LDH release in the presence of sevoflurane 2. 2% or HFIP 4 mM was only visible by +18% and 20%, respectively. Sevoflurane did not influence oxygen consumption rate or extracellular acidification rate, whereas HFIP reduced OCR and raised ECAR, an effect similar to oligomycin, an adenosine triphosphate synthase inhibitor. When blocking the conversion of sevoflurane into HFIP, the risks of sevoflurane were mitigated, but not of HFIP u2013. Conclusion: Our results show that sevoflurane metabolism converts into HFIP is an important factor in cardiomyocyte postconditioning following hypoxia/reoxygenation injury.

Source link: https://doi.org/10.1016/j.bjao.2022.100116


Electrophysiological Changes of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes during Acute Hypoxia and Reoxygenation

The most common cardiovascular disease and a significant burden on healthcare worldwide, is Ischemic heart disease. In our latest cell culture assembly, we used human-induced pluripotent stem cell-derived cardiomyocytes to model acute ischemia-reperfusion. Hypoxia was induced by 0% O2 gas for three hours and reoxygenation with 19% O2 gas for 24 hours in serum- and glucose-free medium in this research, and glucose-free medium for 24 hours. In conclusion, the hiPSC-CMs reproduced many common alterations of adult CMs during ischemia and reperfusion, proving their usefulness as a human-based model of acute cardiac ischemia-reperfusion.

Source link: https://doi.org/10.1155/2022/9438281


Small molecule-mediated rapid maturation of human induced pluripotent stem cell-derived cardiomyocytes

The asiatic acid and GW501516 were two small molecule activators of the peroxisome proliferator-activated receptor uk23b2/u03b2/u03b2 and gamma coactivator 1-alpha pathway. Methods and Results Monolayers of iPSC-CMs were incubated with AA or GW every other day for ten days, resulting in an increase in the expression of FA metabolism-related genes and mitochondrial markers. The mitochondrial respiratory chain inhibitors' responsiveness to the mitochondrial respiratory chain inhibitors by an AA-treated iPSC-CMs increased and demonstrated greater flexibility in substrate utilization, as substrate utilization increased. In addition, structural stability after therapy was enhanced after therapy, as shown by an increase in mRNA expression of sarcomeric-related genes and elevated nuclear polyploidy in AA-treated samples. In addition, therapy resulted in increased ion channel gene expression and protein levels.

Source link: https://doi.org/10.1186/s13287-022-03209-z


Investigating the effect of Shenmai injection on cardiac electrophysiology and calcium signaling using human-induced pluripotent stem cell-derived cardiomyocytes

Traditional Chinese medicine injection refers to the use of modern technology to produce Chinese patent medicines in injectable forms, which reduces the initiation time of traditional Chinese medicine. Although there have been clinical trials in which Shenmai injection was used to diagnose cardiovascular disease, there have been no pharmacological studies that investigate the drug's effectiveness in vitro or the underlying mechanisms. In human-induced pluripotent stem cell-derived cardiomyocytes, we wanted to systemically assess the effectiveness and investigating the mechanisms of SMI in modulating electrophysiology and calcium signaling by using a microelectrode array and a genetically encoded Ca2+ indicator, GCaMP6s, respectively. Conclusions: To determine the chronic effects of TCM, we first used the Ca2+ barometer. We found that SMI therapy can modify electrophysiology and calcium signaling, cardiac muscle contraction, and the cell cycle pathway in hiPSC-CMs.

Source link: https://doi.org/10.1016/j.bbrep.2022.101407


LSD1 in beige adipocytes protects cardiomyocytes against oxygen and glucose deprivation

However, the role of LSD1 in the adipogenic differentiation of beige adipocytes in EpAT is unclear, as well as its effect on oxygen and glucose deprivation in injured cardiomyocytes. LSD1-shRNA lentivirus infection knocked down 3T3-L1 cells, knocking down LSD1-L1 cells. For OGD therapy, the cardiomyocytes co-cultured with beige adipocytes was used. Results: LSD1 depletion was attributed to the onset of age-dependent adipocyte loss in mice EpAT. Conclusion: The decreased expression of LSD1 in 3T3-L1 cells in mice EpAT was correlated with age-dependent angiogenesis of beige adipocytes. The protective effect of beige adipocytes on OGD-injured cardiomyocytes is reduced by the knockdown of LSD1 in adipocytes.

Source link: https://doi.org/10.22038/ijbms.2022.65006.14313

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions