ArticleKorean circulation journal2025
YAK577 Attenuates Cardiac Remodeling and Fibrosis in Isoproterenol-Infused Heart Failure Mice by Downregulating MMP12.
Article in Korean circulation journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Plant-Derived Polyphenol Salvianolic Acid B Attenuates Cardiomyocyte Pyroptosis by Modulating the MMP12-NLRP3 Signaling Axis.Food science & nutrition · 2026Article
- Review
- YAK577 Attenuates Vascular Calcification by Targeting an MMP14-NOX2/ROS Axis in VSMCs and a Vitamin DAntioxidants (Basel, Switzerland) · 2026Article
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Knockdown of the Long Noncoding RNA ZEB1-AS1 Accelerates Cardiac Hypertrophy via the miR-186-5p/HDAC2 Pathway.Arquivos brasileiros de cardiologia · 2025Article
- Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Recent Insights into the Creation of Histone Deacetylase Inhibitors for the Treatment of Human Diseases.International journal of molecular sciences · 2025Review
- Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3.Scientific reports · 2025Article
- Epigenetic Modulation in Heart Failure: HDAC Inhibitors as Emerging Therapeutic Allies.Korean circulation journal · 2025Article
- Sympathetic overactivation and catecholamine toxicity: mechanisms and therapeutic strategies for neurogenic heart injury following acute ischemic stroke.Frontiers in cardiovascular medicine · 2025Review
- Epigenetic modifications in cardiac fibrosis: recent evidence of new pharmacological targets.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
BACKGROUND AND
objectivesHeart failure is a potentially fatal event caused by diverse cardiovascular diseases, leading to high morbidity and mortality. Histone deacetylase (HDAC) inhibitors positively influence cardiac hypertrophy, fibrosis, hypertension, myocardial infarction, and heart failure, causing some side effects. We aimed to investigate the effect of the novel HDAC inhibitor YAK577 on the heart failure mouse model and its underlying mechanism.
methodsNew hydroxamic acid YAK577 was prepared via methyl-2,3-diphenylpropanoate synthesis using carboxylic acids. We used a micro-osmotic pump, including isoproterenol (ISO; 80 mg/kg/day), to induce a heart failure with reduced ejection fraction. Cardiac hypertrophy was assessed by heart weight to body weight ratio and cross-sectional area. The left ventricular (LV) function was assessed by echocardiography. Fibrosis was evaluated using picrosirius red staining. Overexpression and knockdown experiments were performed to investigate the association between HDAC8 and matrix metalloproteinase 12 (MMP12).
resultsYAK577 treatment restored ISO-induced reduction in LV fractional shortening and ejection fraction (n=9-11). YAK577 significantly downregulated cardiac hypertrophy marker genes (natriuretic peptide B,
conclusionsYAK577 acts as a novel heart failure drug through the HDAC8/MMP12 pathway.
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Registered trials
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