Upregulation of endogenous Klotho inhibits pathogenic Wnt/β-catenin signaling and may offer a novel strategy for prevention and treatment of cardiac fibrosis in CKD patients.
We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling.
In conclusion, RASSF1-AS1 inhibits the translation of RASSF1A to exacerbate cardiac fibrosis in mice, indicating a potential application of RASSF1-AS1 as a therapy target for cardiac fibrosis.
In conclusion, RASSF1-AS1 inhibits the translation of RASSF1A to exacerbate cardiac fibrosis in mice, indicating a potential application of RASSF1-AS1 as a therapy target for cardiac fibrosis.
NEW & NOTEWORTHY Ischemia-induced B lymphoma Mo-MLV insertion region 1 homolog (BMI1) significantly promoted cardiac fibrosis and worsened cardiac function in vivo, whereas downregulation of BMI1 decreased cardiac fibrosis and prevented cardiac dysfunction in myocardial infarcted mice.
In conclusion, our results identify FOXM1 as a driver of TGF-β-induced EndMT and underscore the therapeutic potential of targeting FOXM1 for cardiac fibrosis.
These results suggest that the AT1 receptor is involved in the development of cardiac fibrosis by stimulating TNFα/NFκB/IκB-triggered CD44 signaling pathways.
Our findings unraveled the potential of emodin to alleviate cardiac fibrosis <i>via</i> upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.
Our results showed that ellagic acid significantly reduced protein expression of HDAC1, mRNA expression of collagen I, collagen III, MMP-2 and MMP-9 and the area of cardiac fibrosis in MI rats.
These results suggest that the AT1 receptor is involved in the development of cardiac fibrosis by stimulating TNFα/NFκB/IκB-triggered CD44 signaling pathways.
In conclusion, our findings show that the deficiency of miR-214-3p exacerbates cardiac fibrosis and reveal a novel miR-214-3p/NLRC5 axis in the regulation of cardiac fibrosis.
<b>Conclusion:</b> This study demonstrates that CXCR4 pathway contributes to pathogenesis of cardiac fibrosis in dilated cardiomyopathy, and it represents a new potential therapeutic target in heart failure.
In conclusion, miR‑216a was involved in the regulation of TGF‑β‑induced myofibroblast transdifferentiation, suggesting that targeting miR‑216a may aid in developing effective interventions for the treatment of cardiac fibrosis.
Flow cytometry analysis was performed to identify cardiac fibroblasts by examining vimentin, fibronectin (FN) and α-actin expression in human CFs. qRT-PCR and western blot assays were performed to confirm the expression of miR-32-5p, DUSP1 and cardiac fibrosis relevant proteins.
Echocardiography and histological analysis revealed cardiac dysfunction and enhanced cardiac fibrosis in TAC-operated animals; ALDH2 deficiency further aggravated these changes.