ArticleEuropean heart journal2015
Canopy 2 attenuates the transition from compensatory hypertrophy to dilated heart failure in hypertrophic cardiomyopathy.
Article in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Targeting of Pentraxin 3 Alleviated Cardiac Hypertrophy in Mice Induced by Angiotensin II.Clinical and experimental pharmacology & physiology · 2026Article
- Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential.Cell stress · 2026Article
- HIF-mediated hierarchical hypoxic adaptation, a novel paradigm in heart failure pathogenesis: is there a role for targeted therapies?Frontiers in pharmacology · 2026Review
- Identification of PANoptosis-Related Biomarkers in Hypertrophic Cardiomyopathy: Insights from Multi-Omics Analysis.Journal of inflammation research · 2026Article
- Cardiomyocyte-Specific RNF128 Attenuates Pathological Cardiac Hypertrophy Progression by Stabilizing SERCA2a through Lys63-Linked Polyubiquitination.Theranostics · 2026Article
- The role of canopy family proteins: biological mechanism and disease function.Molecular biology reports · 2025Review
- Identification and validation of differentially expressed disulfidptosis-related genes in hypertrophic cardiomyopathy.Molecular medicine (Cambridge, Mass.) · 2024Article
- Liraglutide ameliorates TAC-induced cardiac hypertrophy and heart failure by upregulating expression level of ANP expression.Heliyon · 2024Article
- Impaired autophagy flux contributes to enhanced ischemia reperfusion injury in the diabetic heart.Autophagy reports · 2024Article
- CNPY2 protects against ER stress and is expressed by corticostriatal neurons together with CTIP2 in a mouse model of Huntington's disease.Frontiers in molecular neuroscience · 2024Article
- A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Prolyl Hydroxylase Inhibitors: a New Opportunity in Renal and Myocardial Protection.Cardiovascular drugs and therapy · 2022Review
- Chronic intermittent hypoxia accelerates cardiac dysfunction and cardiac remodeling during cardiac pressure overload in mice and can be alleviated by PHD3 overexpression.Frontiers in cardiovascular medicine · 2022Article
- Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling.Oxidative medicine and cellular longevity · 2022Review
- Pinocembrin ameliorates post-infarct heart failure through activation of Nrf2/HO-1 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- Article
- The regulatory roles of p53 in cardiovascular health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- MiR-221-3p targets Hif-1α to inhibit angiogenesis in heart failure.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Berberine Attenuates Cerebral Ischemia-Reperfusion Injury Induced Neuronal Apoptosis by Down-Regulating the CNPY2 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Mutual Antagonism of Hypoxia-Inducible Factor Isoforms in Cardiac, Vascular, and Renal Disorders.JACC. Basic to translational science · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsA mismatch between adequate angiogenesis and overgrowth of myocytes may be a critical mechanism controlling the transition from adaptive hypertrophy to heart failure. Canopy 2 (CNPY2) was recently identified as a secreted, HIF-1α-regulated angiogenic growth factor. As angiogenic factors play important roles in the development of myocardial hypertrophy, we investigated the role of CNPY2 in molecular and functional changes during development of chronic heart failure using cardiac-specific transgenic (TG) mice that overexpress human CNPY2. METHODS AND
resultsWe generated TG mice that constitutively express CNPY2 in the myocardium. Cardiomyopathy was induced in TG and wild-type (WT) mice by transverse aortic constriction (TAC). WT mice developed significant ventricular hypertrophy at 4 weeks and severe dilatation and heart failure at 12 weeks after TAC. However, TG mice preserved much better cardiac structure and function, with less severe ventricular dilatation and markedly reduced cardiac apoptosis and fibrosis following TAC. Excess CNPY2 in TG mice prevented significant loss of vasculature up to 12 weeks after TAC injury, resulting in a better local myocardial environment that facilitated myocyte survival and prevented excessive matrix remodelling compared with WT mice. TG mice had less accumulation of endogenous tumor suppressor p53 after TAC, indicating intrinsic activation of the p53-mediated repression of HIF-1α, and Cnpy2 was diminished in TG mice compared with WT controls.
conclusionOur study showed a correlation between downregulation of endogenous mouse Cnpy2 and p53-mediated HIF-1α inhibition during late-stage hypertrophic development. Additional CNPY2 attenuated the transition from compensatory hypertrophic response to maladaptive ventricular dilatation and heart failure.
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