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Cardiac Hypertrophy Signaling - Crossref

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Last Updated: 13 August 2022

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Changes of β-adrenergic signaling in compensated human cardiac hypertrophy depend on the underlying disease

The inhibitory G protein u03b1-subunit measurement was unchanged in HOCM, although the inhibitory G protein u03b1-subunit was raised. In comparison, G1b1 i-2 protein in AoSt remained unchanged, but G s u03b1 protein was increased, although G b1's u03b1 protein was unchanged, but G s u03b1 protein was unchanged, but G s u03b1 protein was unchanged, but G s u03b1 protein was increased. Both forms of hypertrophy are linked to u03b2-adrenoceptor downregulation, but with different changes at the G protein level that occur before clinical heart disease occurs due to progressive dilatation of the left ventricle and not due to elevated plasma catecholamine levels, in conclusion.

Source link: https://doi.org/10.1152/ajpheart.2000.278.6.h2076


Metabolic reprogramming via PPARα signaling in cardiac hypertrophy and failure: From metabolomics to epigenetics

Our understanding of metabolic remodeling in cardiac hypertrophy and failure has been expanded by experiments using omics-based technologies. Metabolic reprogramming via PPAR-u03b1 signaling in heart failure propagates into myocardial energetics. PPAR u03b1's transcriptional activities are highly coordinated and flexible, but still highly coordinated. This paper summarizes our current understanding of the PPARu03b1 regulatory mechanisms in cardiac metabolism and the potential role of PPARu03b1 in epigenetic changes in the diseased heart. In addition, we explore how metabolomics can help with a better understanding of the role of PPAR-u03b1 in cardiac hypertrophy and failure.

Source link: https://doi.org/10.1152/ajpheart.00103.2017


Asiatic Acid Alleviates Ang-II Induced Cardiac Hypertrophy and Fibrosis via miR-126/PIK3R2 signaling

Asiatic acid has a strong calming effect on cardiac hypertrophy, according to new studies. Here, this research was designed to determine whether AA's anti-hypertrophy effect is partially miR-126 dependent, and that it should determine whether or not miR-126 is dependent on AA-126. MethodsMale Sprague Dawley rats were injected with osmotic minipumps for four weeks and were treated with AA by oral gavage, with AA. And, the effects of AA on the miR-126 and PI3K/AKT signaling pathway were investigated. MiR-126 was also found that it directly attacked PIK3R2 by miR-126.

Source link: https://doi.org/10.21203/rs.3.rs-269028/v1


Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway

With transverse aortic constriction rats, we investigated the effects of Wenxin Keli on the Calcium/Calmodulin dependent signal transduction pathway. However, WXKL treatment reduced the protein content and phosphorylation of CaMK II, as well as raising the protein level and phosphorylation of PLB and RYR2 phosphorylation. The accumulation of type III collagen fibers in WXKL has also decreased. In conclusion, WXKL may improve cardiac function and reduce arrhythmia by regulating the CaMK II signal transduction pathway.

Source link: https://doi.org/10.1155/2017/1569235

* 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