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In particular, we take a closer glance at the role of nutrient sensing pathways and the potential role of cap-independent translation mediated by the modulation of mTOR pathways in the regulation of cardiac gap junctions and other related aspects of CM maturation. In addition, the relationship between the developing neonatal human heart and brown adipose tissue as the key source of neonatal thermogenesis and its endocrine function on CM formation is another topic that is worth investigating. The latest research has helped to better understand CM maturation by revealing some of the key factors involved in maturation and establishment of metrics for assessment of maturation, which is especially relevant for future studies into in vitro PSC-CMs maturation.
Source link: https://doi.org/10.3389/fcvm.2022.967659
Both challenge and promise were present in this disease research using human-induced pluripotent stem cell-derived cardiomyocytes. Although patient-derived iPSC-CMs provide a unique opportunity for disease modeling with isogenic cells, the issue is that these cells also have specific characteristics that make it less akin to adult cardiomyocytes. Human cells in vitro modeling heart disease are bringing us closer to the possibility of modeling heart disease using human cells.
Source link: https://doi.org/10.3389/fcvm.2022.966094
However, the similarities and differences between conventional 2-dimensional culture and 3-dimensional organoid culture frameworks for CM differentiation have been incompletely clarified. We conducted a comparative study between 2D monolayer and direct 3D cardiac organoid differentiation from hiPSCs during the sequential differentiation stages to see how each culture system influences CMs' properties. Despite identical differentiation cues being used to hiPSCs, the 3D differentiation system demonstrated greater mesoderm commitment and cardiac induction than 2D monolayer differentiation. The present study explores the 2D and 3D culture techniques for CM differentiation from iPSCs, as well as 3D cell culture as an effective way to encourage and observing cardiac maturation.
Source link: https://doi.org/10.51335/organoid.2022.2.e14
Myocardial infarction is a common cardiovascular disease characterized by permanent heart disease and scar tissue formation due to myocardial ischemia. Pluripotent stem cell-derived cardiomyocytes transplanted into various cell populations indefinitely are able to proliferate and distinguish, and stem cell transplanted into areas of injury can treat part of the injuries and are considered one of the most promising cell replacement therapies.
Source link: https://doi.org/10.3389/fbioe.2022.973496
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 human-u2010induced pluripotent stem cell cultureu2013derived cardiomyocytes, the majority of which have focused on genotype correlations and drug screening, and drug screening. This paper sought to compare various BrS models in order to gain a better understanding of the contributions of humanu2010induced pluripotent stem cellu2013derived cardiomyocytes in current BrS research and personalized medicine at a later stage.
Source link: https://doi.org/10.1161/jaha.121.024410
Although pluripotent stem cell-derived cardiomyocytes have been a new source of heart repair, the clinic application is hampered by a lack of maturity. However, the results of 3D nanofibrous scaffolds in the maturation of iPSC-CMs remain unclear. 3D-shaped iPSC-CMs with increased calcium transient kinetics, resulting in increased calcium peak transient amplitude and maximum upstroke speed, as well as increased maximum upstroke velocity. These findings also showed that combining stem cells with scaffolds could be a viable option to increase the myocardium bioengineering process.
Source link: https://doi.org/10.3389/fcell.2022.875278
Objectives: The aim of this research was to establish a cellular model of BrS in the presence of a CACNB2 variant of uncertain importance using human-induced pluripotent stem cell-derived cardiomyocytes and test drug effects using this model. Methods and findings: This paper used cells from a patient with Brugada syndrome and recurrent ventricular fibrillation that had a missense version of CACNB2 as well as three healthy individuals. The study used these cells obtained from skin biopsies of healthy people and the BrS patient as well as CRISPR/Cas9 modified cells. Compared to the healthy control hiPSC-CMs, the BrS patient's hiPSC-CMs had a significant decreased L-type calcium channel current. Compared to healthy hiPSC-CMs, the CACNB2 of the BrS-patient's hiPSC-CMs was significantly reduced.
Source link: https://doi.org/10.3390/ijms23158313
Abstract Background Human induced pluripotent stem cell-derived cardiomyocytes from the onset of regenerative medicine and in vitro screening. Despite displaying primary cardiomyocyte phenotypic features, they more closely match fetal/neonatal cardiomyocytes and are thus young, and mature cardiomyocytes tend to depend on glucose as a source of metabolic fuel, while mature cardiomyocytes mainly use oxidative phosphorylation of fatty acids. Increasing evidence, as a transcription factor, established the critical role of Nrf2 in the regulation of energy metabolism, which specifically controls the expression of mitochondrial respiratory complexes. Methods by knock-down and activation of Nrf2 were investigated by analysis of morphological and functional changes related to mitochondrial maturation and cell differentiation. Cell maturation was slowed as a result of the inhibition of Nrf2. The findings revealed that the inhibition of Nrf2 contributed to cell maturation's slowing. According to a bioinformatics review, Nrf2 also stimulates the expression of myocardial ion channels in addition to metabolism-related genes.
Source link: https://doi.org/10.21203/rs.3.rs-140415/v1
Treatment-induced cardiotoxicity is a common cause of acute and late onset morbidity and mortality in cancer patients on antineoplastic drugs such as melphalanu2014increasing clinical case studies have shown that it can cause cardiotoxicity such as severe arrhythmias and heart failure. As the mechanism by which melphalan impairs cardiac cells is poorly understood, here we investigated cardiomyocytes isolated from human induced pluripotent stem cells to investigate the cellular and molecular mechanisms of melphalan-induced cardiotoxicity, as well as potential target therapeutics. According to the proteomic and transcriptomic results, melphalan-induced cardiotoxicity was also implicated in multiple other signaling pathways, including the p53 and transforming growth factor-u03b2 signaling pathways were also implicated in melphalan-induced cardiotoxicity. This report provides a unique resource of melphalan-induced cardiotoxicity data worldwide, as well as potential new clinical mechanism-based approaches to prevent and treat melphalan-induced cardiotoxicity.
Source link: https://doi.org/10.21203/rs.3.rs-45895/v2
Abstract Background: Abstract Background: Therapeutic-induced cardiotoxicity is a common noncancer-related cause of acute and late onset morbidity and mortality in cancer patients on antineoplastic drugs such as melphalan—u2014increasing clinic case reports have shown that it can cause cardiovascular arrests, severe arrhythmias, and heart failure in cancer patients. Here we looked to analyze cellular and molecular mechanisms of melphalan-induced cardiotoxicity and potential therapeutic therapeutics as the mechanism by which melphalan impairs cardiac cells remains poorly understood. According to the proteomic and transcriptomic results, multiple other signaling pathways, including the p53 and transforming growth factor-u03b2 signaling pathways, were also implicated in melphalan-induced cardiotoxicity. This review provides unique resource of the global transcriptomic and proteomic data for melphalan-induced cardiotoxicity, which may lead to the discovery of new clinical mechanisms-based targets to prevent and treat melphalan-induced cardiotoxicity.
Source link: https://doi.org/10.21203/rs.3.rs-45895/v1
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