ArticleAmerican journal of translational research2018
Xin Fu Kang oral liquid inhibits excessive myocardial mitophagy in a rat model of advanced heart failure.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- FGF21-FGFR1 signaling protects against cardiac hypertrophy by regulating PINK1-mediated mitophagy pathway.Journal of advanced research · 2026Article
- The core mechanism of traditional Chinese medicine in improving myocardial fibrosis: restoring the dynamic balance of mitochondrial quality control.Frontiers in cardiovascular medicine · 2026Review
- Xin-Fu-Kang oral liquid improves cardiac function and attenuates miR-223-associated NF-κB/NLRP3 pyroptotic signaling in chronic heart failure.Frontiers in pharmacology · 2025Article
- Sacubitril/valsartan mitigates cardiac remodeling, systolic dysfunction, and preserves mitochondrial quality in a rat model of mitral regurgitation.Scientific reports · 2023Article
- Relationship between ferroptosis and mitophagy in cardiac ischemia reperfusion injury: a mini-review.PeerJ · 2023Review
- FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy.Cell & bioscience · 2022Article
- Role of Mitophagy in Cardiovascular Disease.Aging and disease · 2020Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure caused by myocardial infarction is a common cardiovascular disease with high mortality rate. Myocardial mitophagy is involved in the process of occurrence and development of heart failure. In this study, we aimed to investigate the effects of Xin Fu Kang (XFK) oral liquid on myocardial mitophagy in a rat model of advanced heart failure. The rat model of advanced heart failure was established by ligating the left anterior descending (LAD) artery for eight weeks. Captopril and XFK were given by gavage separately. Cardiac function and myocardial mitochondrial ultrastructure were observed. Co-localization of mitophagy-related proteins was observed by fluorescence microscopy. Quantitative polymerase chain reaction (qPCR) and western blotting were performed for mRNA and protein level detection, respectively. Compared with the sham group, advanced heart failure group showed a significant reduction in cardiac function with destruction of myocardial mitochondrial structure. Co-localization between mitophagy-related proteins (parkin, p62, and LC3) and mitochondria increased significantly. The mRNA and protein levels of pink1, parkin, p62, and LC3 indicated that excessive mitophagy was observed in the rat model of advanced heart failure. XFK intervention could regulate pink/parkin pathway and inhibit excessive mitophagy.
Indexed as
Identifiers
30416661PMC6220223What OpenQuestion holds
Registered trials
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