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Heart disease and mortality worldwide are the leading cause of morbidity and mortality. TLR2 was found to be elevated in mouse heart tissues with HF under ISO condition. TLR2 levels in the model under ISO stimulation were found by cardiomyocytes and macrophages, which were later identified as the key cellular sources of the increased TLR2 levels. Using TLR2 knockout mice and bone marrow transplantation models, the effect of TLR2 deficiency on ISO-induced cardiac remodeling was determined. TLR2-mediated cell inflammation and remodeling were shown by clinical micromyocytes and macrophages in vitro, and TLR2 knockdown significantly reduced ISO-induced cell proliferation and remodeling by MAPKs/NF-u03baB signaling. ISO remarkably enhanced the TLR2-MyD88 synthesis in the above cells in a TLR1-dependent manner. TLR2 may be a target for the reduction of chronic adrenergic stimulation-associated HF, according to our summary. In addition, this research discusses the possibility of TLR2 as a new target for heart failure under ISO stimulation.
Source link: https://europepmc.org/article/MED/36583707
According to the previous study, cardioprotection by I/Post may have diminished in aged mice, and hypoxic postconditioning lacked a protective role in senescent cardiomyocytes, which was associated with low expression of long-coding RNA H19. Neonatal cardiomyocytes were isolated from 2-day-old Sprague Dawley rats, and senescence was caused by D-galactose, followed by stimulation of hypoxia-reoxygenation and H/Post. Cell viability and the Bcl-2/Bax protein ratio were used to determine hypoxic injury. Total m6A levels were measured using a colorimetric m6A RNA Methylation Quantification Kit and the m6A modified and differentially expressed mRNA was determined by methylated RNA immunoprecipitation. In aged cardiomyocytes, we found that H/Post raised m6A methylation and reduced RNA methylase alkB homolog 5 expression. In addition, ALKBH5 coerced STAT3 expression by broadcasting its m6A modification and lncRNA H19/miR-124-3p. The low expression of STAT3 in senescent cardiomyocytes in ALKBH5 also reduced the H/Post injury induced by the lack of STAT3 in senescent cardiomyocytes, as shown by the absence of STAT3 in senescent cardiomyocytes.
Source link: https://europepmc.org/article/MED/36609501
Diabetic cardiomyopathy has been shown to elevate the risk of fatal ventricular arrhythmia. Despite the negligible SGLT2 presence in cardiomyocytes, the beneficial effects of the selective sodium-glucose co-transporter 2 inhibitor's selective sodium-glucose co-transporter 2 inhibitor in cardiac medicine have yet to be fully investigated in the context of anti-arrhythmic therapy, particularly its direct cardioprotective effects. We performed echocardiography and hemodynamic studies, Ca 2+ handling, and protein expression in C57BLKS/J-lepr db/db mice and their non-diabetic Lepr db/+ littermates. Diabetic cardiomyocytes increased spontaneous Ca 2+ events and reduced sarcoplasmic reticulum Ca 2+ content, as well as impaired Ca 2+ transient, all of which were normalized with EMPA therapy. In conclusion, EMPA reduced ventricular arrhythmia inducibility by normalizing intracellular Ca 2+ transport, and we hypothesized that this result was, at least partially due to the reduction of glucose uptake into cardiomyocytes.
Source link: https://europepmc.org/article/MED/36607794
Previous research has shown that miR-322 can regulate the function of various stem cell types. Celf1 can play a vital role in stem cell differentiation and may be a potential target of miR-322 in ESCs-u2019 differentiation, and may be a potential target of miR-322 in ESCs-u2019 differentiation. MiR-322 was shown to boost NKX-2. 5, MLC2V, and u03b1-MHC mRNA expression in vitro, according to RT-PCR results, indicating that miR-322 could aid in the differentiation of ESCs into cardiomyocytes in vitro. In addition, the discovery that miR-322 expression knockdown could inhibit ESCsu2019 differentiation toward cardiomyocytes in cultured ESCs in vitro. MiR-322 was shown to reduce celf1 protein expression in the Western blot study, but western blot results showed that miR-322 could reduce celf1 protein expression.
Source link: https://europepmc.org/article/PPR/PPR593254
Objective This research aims to decode the proteomic signature of cardiomyocytes in response to lncRNA Ftx knockdown and overexpression by proteomic analysis, as well as the biological role of lncRNA Ftx in cardiomyocytes. paraphrasedoutput:METHODS: The expression of the lncRNA Ftx in cardiomyocytes cultured in vitro was modified, and protein changes in cardiomyocytes 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 identified in the lncRNA Ftx overexpression group, while 67 up-regulated proteins and 54 down-regulated proteins are identified, including 33 upregulated proteins and 54 down-regulated proteins. The lncRNA Ftx is involved in regulating cardiomyocyte apoptosis and ferroptosis, as well as cell energy metabolism, according to a functional clustering analysis of differential genes. Conclusions This research shows that lncRNA Ftx plays a vital role in cardiomyocytes and may play a role in the occurrence and development of various myocardial disorders.
Source link: https://europepmc.org/article/MED/36604692
Diabetic cardiomyopathy is a myocardial disorder that is unrelated to other cardiovascular disorders such as coronary heart disease, hypertension, etc. We investigated the causes of lipid metabolism disruption in DCM in HL-1 cells in this study. We found that canagliflozin significantly reduced the expression of inflammatory factors cyclooxygenase-2 and inducible nitric oxide synthase in both biological informatics and Western blotting studies. Ferroptosis is caused by lipid peroxidation. By measuring intracellular Fe 2+ content, metabolic oxygen species, malondialdehyde, reduced glutathione, and mitochondrial membrane potential, we established ferroptosis in cardiomyocytes.
Source link: https://europepmc.org/article/MED/36614295
Diabetic cardiomyopathy is a myocardial disease that is unrelated to other cardiovascular disorders, such as coronary heart disease, hypertension, and others. DCM in HL-1 cells was the product of lipid metabolism change in this study. We found that canagliflozin significantly reduced the expression of inflammatory factors cyclooxygenase-2 and inducible nitric oxide synthase, both in bioinformatics and Western blotting analysis. By measuring intracellular Fe2+ content and urinaryme concentrations, reduced glutathione, and mitochondrial membrane potential, we established ferroptosis in cardiomyocytes.
Source link: https://europepmc.org/article/MED/PMC9821072
However, the role of LSD1 in the adipogenic differentiation of beige adipocytes in EpAT remains unclear, as well as its role on oxygen and glucose deprivation in injured cardiomyocytes. Materials and methods The tissues of young mice and elder mice were collected for immunohistochemical staining. LSD1-shRNA lentivirus infection destroyed LSD1-L1 cells in 3T3-L1 cells, knocking them down. For OGD therapy, the cardiomyocytes co-cultured with beige adipocytes were used. EpAT: The decrease of LSD1 was attributed to the age-dependent absence of beige adipocytes in mice. The development of beige adipocytes and differentiation of beige adipocytes was hindered by the adipogenic differentiation of 3T3-L1 cells and cell differentiation of beige adipocytes by LSD1 knockdown. The down-regulation of LSD1 in 3T3-L1 cells reduced the protective effect of mature adipocytes on OGD-injured cardiomyocytes. Conclusions The reduced expression of LSD1 in mice was associated with age-dependent adipocyte maturation. LSD1 knockdown in adipocytes has reduced the protective effect of beige adipocytes on OGD-injured cardiomyocytes.
Source link: https://europepmc.org/article/MED/36594068
Human induced pluripotent stem cell-derived cardiomyocytes are less active than those of normal adult cardiomyocytes, and their use in disease therapy and regenerative medicine is limited. We investigated the role and regulatory mechanisms of SIRT3 in energy metabolism in HiPSC-CMs in this study. In summary, SIRT3 regulated energy and stimulated metabolism renewal by targeting the OPA1-controlled mitochondrial dynamics in HiPSC-CMs, and targeting SIRT3 can have unforeseen results in cardiovascular disease treatment and transplantation of HiPSC-CMs.
Source link: https://europepmc.org/article/MED/36596388
However, the specific function of CXCR4 in cardiomyocytes is uncertain. It was hypothesized that CXCR4 triggering in cardiomyocytes antagonizes antagonization in cardiomyocytes, causing heart abnormalities in 2011-u2013. CXCR4 fl/fl and MHC+/u2011 mice were created by crossing CXCR4 fl/fl and MHCu2011Cre +/-u2011 mice. SDF20111 therapy markedly attenuated Isou2011-induced hypercholemia and decrease in phosphorus, as shown by the knockdown of CXCR4 or cou2011 treatment with Gi inhibitors. During u03b2u2011 adrenergic stress, CXCR4 enhances cardiomyocyte growth and heart health. In conclusion, CXCR4 promotes cardiomyocyte proliferation and heart function.
Source link: https://europepmc.org/article/MED/36579657
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