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RSG has been shown to be an elevated risk of cardiovascular disease in studies. RSG's activation of PPAR3 by RSG boosted the endocannabinoid system, a membrane lipid signaling device that triggered cardiac hypertrophy. Importantly, PPARu03b3 activation in the CB1 promoter area increased the expression of cannabinoid receptor type 1 by an identified binding site for PPARu03b3. These findings revealed that the ECS serves as a novel object of PPAR03b3 and that the AEA/CB1/mTOR axis mediates RSG-induced cardiac remodeling.
Source link: https://doi.org/10.1038/s41401-022-00858-x
Fischmeister and colleagues explore heart and cGMP signaling in cardiomyocytes and how they can be improved in heart failure. Although PDE3 inhibitors, such as milrinone or enoximone, have been used medically to enhance systolic function and reduce acute HF symptoms, chronic use of PDE3 inhibitors has been proving to be fatal. We introduce cAMP and cGMP signaling in cardiomyocytes and heart muscle tissue, as well as pathological cardiac hypertrophy and HF in this Review. In addition, research from preclinical studies and clinical studies pointing to the use of inhibitors or activators of particular PDEs that may have therapeutic value in HF is also included in this review.
Source link: https://doi.org/10.1038/s41569-022-00756-z
Melatonin has been shown to reduce heart hypertrophy and fibrosis by increasing sleep and melatonin levels in the body, according to new studies. To determine the effects of nanoparticles on myocardial fibrosis and hypertrophy in the heart, a mouse model of pressure overdriven cardiac hypertrophy was used. Mel/CHP@AuNPs have a diameter of 220. 5 nm and negative zeta potential of 20. 18 mV, and a potential of 20. 28 mV. In the Mel/CHP@AuNPs and magnetic characteristics that showed no residual magnetization or coercivity, as shown by the design of magnetic hysteresis curves, an excellent encapsulation capacity for AuNPs and Melatonin was discovered.
Source link: https://doi.org/10.1007/s10924-022-02452-y
We created a novel SIRT3 activator, 3--7-hydroxy-2H-chromen-2-one, in this study through structural optimization of the first SIRT3 agonist C12. We demonstrated that SZC-6 was directly bound to SIRT3 with a K_d value of 15 bcM, as well as increased SIRT3 deacetylation rate with a EC_50 value of 23. 2 g/m5M, increasing SIRT3 deacetylation activity with EC_50 value of 33. 2 u00b5 million. In wild-type mice, ISO treatment dose-dependently restored diastolic and systolic cardiac function, but not in SIRT3 knockdown mice. In ISO-treated NRCMs, we also reported that activation of SIRT3 by SZC-6 increased ATP production and rate of mitochondrial oxygen consumption, as well as reduced ROS. These findings, taken together, reveal that SZC-6 is a novel SIRT3 agonist with potential use in the treatment of cardiac hypertrophy partially by the LKB1-AMPK pathway.
Source link: https://doi.org/10.1038/s41401-022-00966-8
In a rat model of hyperthyroidism-induced cardiac hypertrophy, the present research was intended to investigate LCZ696's therapeutic sensitivity and potential contributions of microRNA regulation. Rats from six different groups were randomly assigned to four separate groups: control, cardiac hypertrophy, CH+ valsartan, and CH + LC696. Compared to CH group rats, LCZ696 or valsartan dramatically reduced hemodynamic abnormalities, normalized serum natriuretic peptide, fibroblast growth factor-23, and cardiac inflammatory markers. A LCZ696 or valsartan treatment has also normalized myocardial expression levels of autophagy enzymes, fibrotic markers, PPAR-u03d2, mir-377, and let-7b.
Source link: https://doi.org/10.1038/s41598-022-18860-y
Background According to research done on animals and humans in vitro and in vivo, heart disease could result from a deletion in the core clock gene BMAL1. We found a potential correlation between BMAL1 and cardiac hypertrophy in the current study. Methods By Ang II, primary cultured neonatal rat cardiomyocytes were stimulated by Ang II. In addition, gain- and loss-of-function studies reported that BMAL1 plays an effect on Ang II-induced cardiac hypertrophy. Ang II-induced cardiac hypertrophy was reduced as a result of reduced BMAL1 expression, which was reduced. In addition, although BMAL1 overexpression in hypertrophic cardiomyocytes could not prevent hypertrophy, it did reduce the apoptosis of hypertrophic cardiomyocytes after Ang II had provoked it. Cardiomyocytes were particularly resistant to the effects of Ang II on oxidative stress, autophagy, and cardiac fibrosis. Conclusions: Our findings showed that overexpression of BMAL1 had stifled cardiac hypertrophy induced by Ang II.
Source link: https://doi.org/10.1186/s12872-022-02822-3
This study seeks to determine the effect of AREG on cardiac hypertrophy and if oxidative stress and apoptosis were involved in cardiac hypertrophy. In vitro, Angiotensin II induced cardiac hypertrophy in mice and neonatal rat cardiomyocytes or HL-1 cells. The rises of Ang II-induced cardiac mass and cardiomyocytes area were stifled as a result of AREG's deregulation. AREG knockdown: The onset of oxidative stress in mice's hearts as a result of Ang II therapy was reduced by AREG's knockdown. AREG downregulation has stifled the production of Ang II-induced Bax and cleaved caspase3 in mice hearts.
Source link: https://doi.org/10.1186/s13062-022-00334-w
paraphrasedum DC's traditional Chinese medicine Zanthoxylum nitidum DC's common active component Nitidine chloride is a common active component. Both ZNE administered in rats and NC mice in mice caused dose-dependent cardiac hypertrophy and dysfunction, according to We, while in Beagles, administration of NC at the middle and high dose resulted in death. We found a decrease in cardiac autophagy in NC-treated mice and neonatal mouse cardiomyocytes, inconsistently. Also, we found that autophagy-related 4B cysteine peptidase can be a potential target of NC, since overexpression of ATG4B stifled the cardiac hypertrophy and reduced autophagy levels in NC-treated mice.
Source link: https://doi.org/10.1038/s41401-022-00968-6
Background Hypertension-induced cardiac hypertrophy is one of the most common pre-conditions that contributes to heart failure. Gene expression in the module was confirmed by the GSE36074 dataset and our transverse aortic constriction mouse model. Lastly, the association of cardiac hypertrophy genes and biomarkers was determined. The ECM-receptor interaction and Oxytocin signaling pathway were both present in GSE18224, which were mainly enrich in biological processes, including collagen fibril organization, cellular response to transforming growth factor-beta stimulation, and involvement in the ECM-receptor interaction and Oxytocin signaling pathway. 387 miRNAs were branded by 257 DEGs, while 177 TFs attacked 71 DEGs. The PPI network had 222 nodes and 770 edges, with 18 genes embedded in the module. Eln and Tgfb3 were both found to be positively correlated with the disease biomarkers, and they were found to be positively linked to the disease biomarker level.
Source link: https://doi.org/10.1186/s12864-022-08778-0
Aim To investigate and compare the mRNA N6-methyladenosine changes in transverse aortic constriction-induced mice hearts and normal mice hearts. RNA-seq and MeRIP-seq were used to find genes with differences in m6A modifications or expression in the transcriptome profile. TAC group methylation levels were higher than those in the control group, respectively. TAC group exhibited higher m6A methylation levels. MeRIP-seq announced that 1179 m6A peaks were methylated and 733 m6A peaks were downmethylated, and 733 m6A peaks were downmethylated, and that biological analysis of these genes demonstrated a strong relationship with heart function.
Source link: https://doi.org/10.1186/s12864-022-08833-w
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