ArticleFrontiers in cardiovascular medicine2021
A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Arterial Stiffness and Heart Failure With Preserved Ejection Fraction.Journal of Korean medical science · 2024Review
- siRNA-mediated reduction of a circulating protein in swine using lipid nanoparticles.Molecular therapy. Methods & clinical development · 2024Article
- Animal models of heart failure with preserved ejection fraction (HFpEF): from metabolic pathobiology to drug discovery.Acta pharmacologica Sinica · 2024Review
- Cardiac sympathetic overdrive, M2 macrophage activation and fibroblast heterogeneity are associated with cardiac remodeling in a chronic pressure overload rat model of HFpEF.Frontiers in pharmacology · 2024Article
- Progress in Orthotopic Pig Heart Transplantation in Nonhuman Primates.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023Article
- Apelin receptor inhibition in ischemia-reperfused mouse hearts protected by endogenous n-3 polyunsaturated fatty acids.Frontiers in pharmacology · 2023Article
- Evaluation of large animal models for preclinical studies of heart failure with preserved ejection fraction using clinical score systems.Frontiers in cardiovascular medicine · 2023Review
- Chronic high-rate pacing induces heart failure with preserved ejection fraction-like phenotype in Ossabaw swine.Basic research in cardiology · 2022Article
- Clinical Phenotypes of Heart Failure With Preserved Ejection Fraction to Select Preclinical Animal Models.JACC. Basic to translational science · 2022Review
- Differential mRNA Expression and Circular RNA-Based Competitive Endogenous RNA Networks in the Three Stages of Heart Failure in Transverse Aortic Constriction Mice.Frontiers in physiology · 2022Article
- Cardioprotective Effects of n-3 Polyunsaturated Fatty Acids: Orchestration of mRNA Expression, Protein Phosphorylation, and Lipid Metabolism in Pressure Overload Hearts.Frontiers in cardiovascular medicine · 2021Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Inhibition of ADAM10 ameliorates doxorubicin-induced cardiac remodeling by suppressing N-cadherin cleavage.Open life sciences · 2021Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure is induced by multiple pathological mechanisms, and current therapies are ineffective against heart failure with preserved ejection fraction (HFpEF). As there are limited animal models of HFpEF, its underlying mechanisms have not yet been elucidated. Here, we employed the descending aortic constriction (DAC) technique to induce chronic pressure overload in the left ventricles of Tibetan minipigs for 12 weeks. Cardiac function, pathological and cellular changes, fibrotic signaling activation, and gene expression profiles were explored. The left ventricles developed concentric hypertrophy from weeks 4 to 6 and transition to dilation starting in week 10. Notably, the left ventricular ejection fraction was maintained at >50% in the DAC group during the 12-week period. Pathological examination, biochemical analyses, and gene profile analysis revealed evidence of inflammation, fibrosis, cell death, and myofilament dephosphorylation in the myocardium of HFpEF model animals, together with gene expression shifts promoting cardiac remodeling and downregulating metabolic pathways. Furthermore, we noted the activation of several signaling proteins that impact cardiac fibrosis and remodeling, including transforming growth factor-β/SMAD family members 2/3, type I/III/V collagens, phosphatidylinositol 3-kinase, extracellular signal-regulated kinase, matrix metalloproteinases 2 and 9, tissue inhibitor of metalloproteinases 1 and 2, interleukins 6 and 1β, and inhibitor of κBα/nuclear factor-κB. Our findings demonstrate that this chronic pressure overload-induced porcine HFpEF model is a powerful tool to elucidate the mechanisms of this disease and translate preclinical findings.
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