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Cardiac Hypertrophy Heart Failure - Crossref

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Last Updated: 13 November 2022

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Cardiac Tissue Factor Regulates Inflammation, Hypertrophy, and Heart Failure in Mouse Model of Type 1 Diabetes

Patients with diabetes are at a higher risk of heart failure. Diabetes' role in HF is less well understood, and current HF products are not particularly efficient in patients with HFpEF. Tissue factor, a transmembrane receptor, plays a key role in diabetes-related immune cell proliferation and atherothrombosis. Type 1 diabetes-induced HF was determined by TF in this research by using wild-type, heterozygous, and low-TF mice. In diabetic WT hearts, we found significant elevations in cardiac TF mRNA and protein levels relative to nondiabetic controls. In comparison to controls, WT diabetic hearts exhibited increased inflammation and cardiac hypertrophy, as well as cardiovascular hypertrophy. However, these changes in cardiac inflammation and hypertrophy in low-TF mice with diabetes were not present in diabetic mice with diabetes in comparison to their non-diabetic controls. TF deficiency was also associated with elevated heart function indicators indicating HFpEF, which was also present in WT mice with diabetes.

Source link: https://doi.org/10.2337/db20-0719


CCL17 acts as a novel therapeutic target in pathological cardiac hypertrophy and heart failure

The prevalence of circulated C-C motif ligand 17 level in an age-stratified healthy population and further community-based cohort together with a heart failure patients study revealed that the circulating C-C motif chemokine ligand 17 level increased with age and correlated with cardiac dysfunction. Our results reveal that chemokine CCL17 is a novel therapeutic target in age-related and Ang IIu2013-induced pathological cardiac hypertrophy and heart failure.

Source link: https://doi.org/10.1084/jem.20200418


Protein Kinase D1 Regulates Cardiac Hypertrophy, Potassium Channel Remodeling, and Arrhythmias in Heart Failure

U2010TAC mice exhibited significantly less cardiac hypertrophy post-u2010TAC and were shielded from early decline in cardiac contractility function, but not the transition to HF at 7 weeks post-u2010TAC. At 8 weeks post-u2010TAC, a tenuation-postponement of ventricular function, increased expression of corresponding K+ channels, and earlier bloom of corresponding K+ channels, which was attenuated in PKD1u2010TAC, which was attenuated in PKD1u2010TAC, which was attenuated in PKD1u2010TAC, accompanied by larger K+ current, stable, inward current, a t u2010TAC, which was u2010TAC, tiger K+ current, corresponding K+ current, ventricular ed corresponding K+ channels. Transient outward current in TAC and sham wildu2010type myocytes in acute PKD induced modest growth in transient outward current, but not alter other K+ currents. The Sham PKD1u2010cKO versus the wild u2010type also showed more transient outward current and faster early action potential repolarization, according to a repolarization survey. Therefore, PKD1 inhibition may be a therapeutic measure to reduce hypertrophy and arrhythmias in HF, but it does not prevent disease progression and reduced contractility in HF.

Source link: https://doi.org/10.1161/jaha.122.027573

* 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