AI Article Synopsis

  • Ferroptosis is a process that can make heart failure worse, and this study looked at how a substance called Astragaloside IV (AS-IV) might help.
  • Researchers used computer methods to find common targets related to heart failure and ferroptosis, focusing on a key target named p53.
  • When CHF rats were treated with AS-IV for 4 weeks, their heart function improved, and signs of heart damage decreased, suggesting AS-IV helps by changing important signaling pathways in the heart.

Article Abstract

Ferroptosis is an important pathological mechanism of chronic heart failure (CHF). This study aimed to investigate the protective mechanism of Astragaloside IV (AS-IV) on CHF rats by integrating bioinformatics and ferroptosis. CHF-related targets and ferroptosis-related targets were collected. After the intersection, the common targets were obtained. The PPI network of the common targets was constructed, and topological analysis of the network was carried out. The target with the highest topological parameter values was selected as the key target. The key target p53 was obtained through bioinformatics analysis, and its molecular docking model with AS-IV was obtained, as well as molecular dynamics simulation analysis. The rat models of CHF after myocardial infarction were established by ligation of left coronary artery and treated with AS-IV for 4 weeks. AS-IV treatment significantly improved cardiac function in CHF rats, improved cardiomyocyte morphology and myocardial fibrosis, reduced mitochondrial damage, decreased myocardial MDA and Fe content, increased GSH content, inhibited the expression of p53 and p-p53, and up-regulated the expression of SLC7A11 and GPX4. In conclusion, AS-IV improved cardiac function in CHF rats, presumably by regulating p53/SLC7A11/GPX4 signaling pathway and inhibiting myocardial ferroptosis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11379966PMC
http://dx.doi.org/10.1038/s41598-024-72011-zDOI Listing

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