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AngII

IGF-1 Protects against Angiotensin II-Induced Cardiac Fibrosis by Targeting αSMA

[Cell Death & Disease] Researchers investigated the roles of IGF-1 signaling during agonist-induced cardiac fibrosis and evaluated the molecular mechanisms in cultured cardiac fibroblasts. They found severe interstitial fibrosis in angiotensin II/phenylephrine infused myofibroblast-specific IGF-1R knockout mice compared to the wild-type mice.

Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes

[International Journal of Molecular Sciences] Investigators demonstrated that the Sphingosine kinase-1 silencing in neonatal mouse cardiomyocytes facilitated their postnatal maturation in both physiological and stress conditions.

GRK5 Is a Regulator of Fibroblast Activation and Cardiac Fibrosis

[Proceedings of the National Academy of Sciences of the United States of America] Researchers demonstrated using adult cardiac fibroblasts that genetic deletion of G protein-coupled receptor kinase 5 inhibits angiotensin II-mediated fibroblast activation.

Angiotensin II-Induced Muscle Atrophy via PPARγ Suppression Is Mediated by miR-29b

[Molecular Therapy-Nucleic Acids] Scientists identified peroxisome proliferator-activated receptor gamma (PPARγ) as a negative regulator of miR-29b, a microRNA that is able to promote multiple types of muscle atrophy. Suppression of miR-29b prevented AngII-induced muscle atrophy both in vitro and in vivo.

Ontogeny of Arterial Macrophages Defines Their Functions in Homeostasis and Inflammation

[Nature Communications] Scientists combined macrophage fate-mapping analysis with single-cell RNA sequencing to establish their cellular identity during homeostasis, and in response to angiotensin-II (AngII)-induced arterial inflammation.

Dual Roles of Chromatin Remodeling Protein BRG1 in Angiotensin II-Induced Endothelial–Mesenchymal Transition

[Cell Death & Disease] BRG1 knockdown or inhibition attenuated angiotensin II-induced endothelial–mesenchymal transition, as evidenced by down-regulation of CDH5, an endothelial marker, and up-regulation of COL1A2, a mesenchymal marker, in cultured vascular endothelial cells.

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