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Cardiac Hypertrophy - DOAJ

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Last Updated: 10 September 2022

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Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics

This research is aimed at determining the key genes and pathways of cardiac hypertrophy using bioinformatics and as well as providing a new target for cardiac hypertrophy detection. Using the online software DAVID, GO functional annotation analysis and KEGG pathway enrichment analysis were performed separately for DEGs. The DEGs were imported into the STRING online database for constructing PPI networks and analyzing DEG-to-DiG interactions. According to GO studies, DEGs were mainly involved in cardiac muscle contraction, blood flow regulation, muscle contraction, muscle contraction, striated muscle contraction, stimulation of heart contraction, regulation of striated muscle contraction, regulation of striated muscle contraction, and tissue remodeling. According to JAK-STAT's study, DEGs played a key role in Th17 cell differentiation, Th1 and Th2 cell differentiation, HIF-1 signaling pathway, pathways in cancer, hematopoietic cell lineage, Chagas disease, and cell adhesion molecules, viral myocarditis, central carbon metabolism in cancer, acute myeloid leukemia, and JAK-STAT signaling pathway.

Source link: https://doi.org/10.1155/2022/2081590


Data Mining Identifies CCN2 and THBS1 as Biomarker Candidates for Cardiac Hypertrophy

Cardiac hypertrophy is a condition that can cause heart failure. We compare the gene expression of hypertrophic human hearts in this paper. The protein-interaction network results showed CCN2 as a central node among the 25 overlapping DEGs, implying that this gene could play a crucial role in cardiac hypertrophy. Multiple biological processes associated with cardiac function and cardiac hypertrophy were discovered by a GO-enrichment review of the 25 DEGs.

Source link: https://doi.org/10.3390/life12050726


Cardiomyocyte-targeted and 17β-estradiol-loaded acoustic nanoprobes as a theranostic platform for cardiac hypertrophy

Abstract Background Theranostic perfluorocarbon nanoprobes have recently attracted attention because of their ability in combining diagnostics and therapeutics in a single device. PCM-E2/PFPs + LIFU therapy has also greatly improved cardiac targeting and circulation time, as well as total length. PCM-E2/PFPs + LIFU inhibited cardiac hypertrophy to a greater degree than other therapies, showing high success in cardiac-targeted delivery and effective cardioprotection. Conclusion Our latest theranostic nanoplatform may be a potential heart disease vector.

Source link: https://doi.org/10.1186/s12951-018-0360-3


Identification of drug repurposing candidates based on a miRNA-mediated drug and pathway network for cardiac hypertrophy and acute myocardial infarction

Abstract Background Cardiac hypertrophy and acute myocardial infarction are two common heart diseases worldwide. Using a computational approach, we also found some strongly delayed miRNA-gene-drug triplets in cardiac hypertrophy and AMI. We characterized the activity score profile for MGDTs in cardiac hypertrophy and AMI. In AMI, we discovered an insulin-like growth factor 1 receptor-related subnetwork in cardiac hypertrophy and a vascular endothelial growth factor A-related subnetwork. We also considered insulin-like growth factor 1 receptor and vascular endothelial growth factor A as two potential drug candidates by utilizing the cardiac hypertrophy and AMI pathways.

Source link: https://doi.org/10.1186/s40246-018-0184-0


Multi-Omics Characterization of a Human Stem Cell-Based Model of Cardiac Hypertrophy

Cardiac hypertrophy is a significant and independent risk factor for heart disease and heart failure caused by cardiac myopathy. Several enriched canonical pathways related to cardiac hypertrophy are identified as early as the earliest time point, e. g. , cardiac hypertrophy signaling. The findings also provide novel insight into the underlying mechanisms of cardiac hypertrophy, and novel putative early cardiac hypertrophy biomarkers have been found that warrant further investigation to determine their potential clinical relevance.

Source link: https://doi.org/10.3390/life12020293


Nanoparticle-Mediated Angiotensin-(1-9) Drug Delivery for the Treatment of Cardiac Hypertrophy

Now, the treatment of neonatal cardiomyocytes in culture with EE/AuNS 2% + Ang-20 percent pNPs reduced the area and perimeter, showing success in preventing norepinephrine-induced cardiomyocyte hypertrophy in myocyte hypertrophy. On the other hand, the introduction of AuNS either directly on the cytotoxicity or on the association capacity of Ang-, implying that the mixed carrier EE/Alg/AuNS pNPs could be used for the delivery of Ang- in the treatment of cardiovascular hypertrophy.

Source link: https://doi.org/10.3390/pharmaceutics13060822


Hyperactivation of mTOR and AKT in a cardiac hypertrophy animal model of Friedreich ataxia

In Friedreich ataxia patients with inadequate iron-sulfur cluster biogenesis due to a lack of functional frataxin and in rare patients with functional impairments of other ISC biogenesis factors, cardiomyopathy is a common cause of death in Friedreich ataxia patients with reduced iron-sulfur cluster biogenesis. Heart and homeostasis control are critical regulators of cardiovascular growth and metabolism with environmental inputs, including nutrients and growth factors. Administration of rapamycin, a specific inhibitor of mTOR signaling, improved the survival of the Fxn cKO mice, providing proof of concept for the possibility of mTOR inhibition in patients with impaired ISC biogenesis. However, AKT phosphorylation remained high in rapamycin-treated Fxn cKO hearts, meaning that parallel mTOR and AKT inhibition may be useful to extend the life and health of ISC deficient individuals.

Source link: https://doi.org/10.1016/j.heliyon.2022.e10371


Protections of transcription factor BACH2 and natural product myricetin against pathological cardiac hypertrophy and dysfunction

Heart failure can be caused by pathological hypertrophic myocardium under persistent adverse environmental stress. Through tail vein injection of AAV9-Bach2, the BACH2 was overexpressed in mice. Myocytes in Neonatal rat ventricular myocytes were isolated and infected with lentivirus to overexpress Bach2 or transfected with siRNA to knock down Bach2. Our results revealed that overexpression of BACH2 enhanced TAC-induced cardiac hypertrophy and failure in mice and mice, as well as decreased isoproterenol-triggered myocyte hypertrophy in NRVMs. BACH2 bound to the promotor region of Akap6 at the -587 site and repressed its expression, the vital scaffold for cardiac hypertrophy and fail signaling pathways, according to further analysis. Myricetin, according to a small molecular natural product library study, could up-regulate expression of Bach2 and simultaneously lower the transcriptional levels of hypertrophic marker genes Bnp and Myh7. In vivo and in vitro, myricetin had a BACH-dependent protective role against cardiac hypertrophy.

Source link: https://doi.org/10.3389/fphys.2022.971424


Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways

In a rat model of hyperthyroidism-induced cardio hypertrophy, the present study was intended to investigate LCZ696's therapeutic value and potential microRNA regulation. Compared to CH group rats, treatment with LCZ696 or valsartan resulted in hemodynamic abnormalities, normalized serum concentrations of natriuretic peptide, fibroblast growth factor-23, and cardiac inflammatory markers. PPAR-u03d2, mir-377, and let-7b were also normalized myocardial expression levels of autophagy markers, fibrotic markers, LCZ696 or valsartan, and let-7b. The improved modulation of miR-377 and let-7b can be attributed to LCZ696's superior efficacy.

Source link: https://doi.org/10.1038/s41598-022-18860-y


Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis

This research seeks to determine the effect of AREG on cardiac hypertrophy and if oxidative stress and apoptosis were involved in cardiac hypertrophy. In vitro, Angiotensin II caused cardiac hypertrophy in mice and neonatal rat cardiomyocytes or HL-1 cells. The rises of Ang II-induced cardiac weight and cardiomyocytes area were limited after AREG's deregulation. The onset of oxidative stress in mice's heart as a result of Ang II therapy was reduced by AREG's knockdown. AREG's downregulation has hampered the growth of Ang II-induced Bax and cleaved caspase3 in mice hearts.

Source link: https://doi.org/10.1186/s13062-022-00334-w

* 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