ArticleActa pharmacologica Sinica2014
Aliskiren ameliorates pressure overload-induced heart hypertrophy and fibrosis in mice.
Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 64 citations in OpenAlex.
- UBA1 promotes cardiac hypertrophy by suppressing autophagy via targeting ATG5 for ubiquitination.Cell communication and signaling : CCS · 2026Article
- Time-restricted feeding attenuated hypertension-induced cardiac remodeling by modulating autophagy levels in spontaneously hypertensive rats.Scientific reports · 2025Article
- The gut microbiota metabolite trimethylamine N-oxide promotes cardiac hypertrophy by activating the autophagic degradation of SERCA2a.Communications biology · 2025Article
- GRIM-19-mediated induction of mitochondrial STAT3 alleviates systemic sclerosis by inhibiting fibrosis and Th2/Th17 cells.Experimental & molecular medicine · 2024Article
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2023Review
- Mllt11 Regulates Migration and Neurite Outgrowth of Cortical Projection Neurons during Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022Review
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- Angiotensin receptor-neprilysin inhibitor attenuates ischemia-hypoxia-induced myocardial injury via inhibition of autophagy.American journal of translational research · 2022Article
- 6-Gingerol protects against cardiac remodeling by inhibiting the p38 mitogen-activated protein kinase pathway.Acta pharmacologica Sinica · 2021Article
- Article
- Beclin-1-Dependent Autophagy of Left Ventricular Cardiomyocytes in SHR and Wistar-Kyoto Rats with Type 1 Diabetes Mellitus.Bulletin of experimental biology and medicine · 2021Article
- Baicalein attenuates cardiac hypertrophy in mice via suppressing oxidative stress and activating autophagy in cardiomyocytes.Acta pharmacologica Sinica · 2021Article
- Exploring Functional Differences between the Right and Left Ventricles to Better Understand Right Ventricular Dysfunction.Oxidative medicine and cellular longevity · 2021Review
- Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives.International journal of molecular sciences · 2020Review
- Advanced glycation end products facilitate the proliferation and reduce early apoptosis of cardiac microvascular endothelial cells via PKCβ signaling pathway: Insight from diabetic cardiomyopathy.Anatolian journal of cardiology · 2020Article
- Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-κB/c-fos signaling pathway.Experimental and therapeutic medicine · 2020Article
- Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.International journal of hypertension · 2020Review
- Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimAliskiren (ALK) is a renin inhibitor that has been used in the treatment of hypertension. The aim of this study was to determine whether ALK could ameliorate pressure overload-induced heart hypertrophy and fibrosis, and to elucidate the mechanisms of action.
methodsTransverse aortic constriction (TAC) was performed in mice to induce heart pressure overload. ALK (150 mg·kg(-1)·d(-1), po), the autophagy inhibitor 3-methyladenine (10 mg·kg(-1) per week, ip) or the PKCβI inhibitor LY333531 (1 mg·kg(-1)·d-(1), po) was administered to the mice for 4 weeks. Heart hypertrophy, fibrosis and function were evaluated based on echocardiography, histological and biochemical measurements. Mechanically stretched cardiomyocytes of rats were used for in vitro experiments. The levels of signaling proteins were measured using Western blotting, while the expression of the relevant genes was analyzed using real-time QRT-PCR.
resultsTAC induced marked heart hypertrophy and fibrosis, accompanied by high levels of Ang II in plasma and heart, and by PKCβI/α and ERK1/2 phosphorylation in heart. Meanwhile, TAC induced autophagic responses in heart, i.e. increases in autophagic structures, expression of Atg5 and Atg16 L1 mRNAs and LC3-II and Beclin-1 proteins. These pathological alterations in TAC-mice were significantly ameliorated or blocked by ALK administration. In TAC-mice, 3-methyladenine administration also ameliorated heart hypertrophy, fibrosis and dysfunction, while LY333531 administration inhibited ERK phosphorylation and autophagy in heart. In mechanically stretched cardiomyocytes, CGP53353 (a PKCβI inhibitor) prevented ERK phosphorylation and autophagic responses, while U0126 (an ERK inhibitor) blocked autophagic responses.
conclusionALK ameliorates heart hypertrophy, fibrosis and dysfunction in the mouse model in setting of chronic pressure overload, via suppressing Ang II-PKCβI-ERK1/2-regulated autophagy.
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