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Cardiac Hypertrophy Signaling - Europe PMC

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Last Updated: 13 August 2022

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GDH promotes isoprenaline-induced cardiac hypertrophy by activating mTOR signaling via elevation of α-ketoglutarate level.

We have the first evidence that glutamate dehydrogenase, an enzyme that promotes the conversion of glutamate into u0251-ketoglutarate, plays a role in isoprenaline-induced cardiac hypertrophy by stimulating a mammalian target of rapamycin signaling in the present study. Following ISO therapy, the expression and function of GDH were enhanced in cultured cardiomyocytes and rat hearts. Both exogenous supplementation and cardiomyocyte hypertrophy were present in mTOR activation and cardiomyocyte hypertrophy. These results provide further insight into the role of GDH in cardiac hypertrophy and suggest it as a potential target for hypertrophy-related cardiomyopathy.

Source link: https://europepmc.org/article/MED/35904584


QiShenYiQi Pill Ameliorates Cardiac Fibrosis After Pressure Overload-Induced Cardiac Hypertrophy by Regulating FHL2 and the Macrophage RP S19/TGF-β1 Signaling Pathway.

However, after cardiac hypertrophy, no approved drugs are available to prevent cardiac fibrosis. Chronic HF is a common problem treated by the QiShenYiQi tablet. Methods: In the present research, a pressure overload-induced cardiac hypertrophy model was developed in rats by inducing ascending aortic stenosis for four weeks. Small interfering RNAs investigated the role of four-and-a-half LIM domains protein 2 in cardiac fibrosis and QSYQ's effects. Results: QSYQ improved cardiac fibrosis after pressure overload-induced cardiac hypertrophy and attenuated cardiomyocyte apoptosis, low FHL2 expression, and TGF-u03b21 release by the injured myocardium. Moreover, QSYQ downregulated TGF-II expression in fibroblasts and slowed Smad protein production and collagen release and deposition, as well as decreased QSYQ's TGF-u03b21 expression. Conclusion: The results revealed that QSYQ reduced myocardial fibrosis after pressure overload, which was mediated by RP S19-TGF-u03b21 signaling and reduced FHL2, thus giving QSYQ as a promising therapy for blocking myocardial fibrosis.

Source link: https://europepmc.org/article/MED/35910357


Metformin Attenuates Cardiac Hypertrophy Via the HIF-1α/PPAR-γ Signaling Pathway in High-Fat Diet Rats.

The main causes of ischemic heart disease are coronary artery disease and cardiac hypertrophy. Left ventricular hypertrophy can result in abrupt CAD. Cardiogenic insufficiency and heart failure can develop long-term and sustained CH, which can lead to cardiac insufficiency and heart failure. To induce CH and explore the potential mechanism of Met on CH, we used high-fat diet rats and H9c2 cells herein. In addition, DFO-regulated the expression of PPAR-u03b3 by DFO treatment, while Ros treatment did not influence the expression of HIF-1u03b1.

Source link: https://europepmc.org/article/MED/35833024


Wnt Signaling Interactor WTIP (Wilms Tumor Interacting Protein) Underlies Novel Mechanism for Cardiac Hypertrophy.

The majority of genetic variants of HCM have been identified in sarcomeric genes to date. WTIP's noncanonical variant is shown here, and we also provide evidence of a role for WTIP in complex disease. WTIP in human cardiac tissue was determined by a weighted gene coexpression network analysis, as well as association studies for WTIP variation and left ventricular hypertrophy. In D rerio, the TIP knockdown caused hypertrophy in neonatal rat ventricular myocytes and increased cardiac hypertrophy, peak calcium, and resting calcium. WTIP emerged as a central coordinate of prohypertrophic networks, according to network analysis, although common variation at the WTIP locus was attributed to human left ventricular hypertrophy. We also show that the gene WTIP gene expression in complex cardiac hypertrophy phenotypes is particularly relevant in orthogonal model systems.

Source link: https://europepmc.org/article/MED/35671065


Yi-Xin-Shu capsule ameliorates cardiac hypertrophy by regulating RB/HDAC1/GATA4 signaling pathway based on proteomic and mass spectrometry image analysis.

Background Cardiac hypertrophy is the most common pathological cause of persistent heart failure. The treatment of ventricular remodeling in CHF is based on mitigation and preventing CH. The Yi-Xin-Shu capsule has been used in clinical treatment of CHF in Asian countries for many decades. Purpose: To determine the effectiveness of YXS in CH and identify its potential therapeutic goals for CH's management of CH. Method Ultrasonic cardiogram was used to determine CH rats' cardiac function. YXS' key target, GATA binding protein 4, was identified as the key target. The expressions of histone deacetylase 1 and retinoblastoma could also be restricted by YXS, according to the results of mass spectrometry image analysis. YXS may attenuate CH by controlling the RB/HDAC1/GATA4 signaling pathway, according to further qualitative studies. Conclusions: This paper publishes the precise mechanism of the YXS' effectiveness against CH for the first time.

Source link: https://europepmc.org/article/MED/35679794

* 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