ArticleActa pharmacologica Sinica2021
Engineered cardiac tissues: a novel in vitro model to investigate the pathophysiology of mouse diabetic cardiomyopathy.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- RAGE in Neutrophils: A Sensor for Pathogen-Associated Structures and Beyond.Biomedicines · 2026Article
- Vascularized Cardiac Tissue Engineering: From Advances in Biofabrication to Translational Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Sympathetic-like-integrated engineered heart tissue models AGEs-induced adverse remodeling.Cardiovascular diabetology · 2026Article
- FTO-Mediated Mitigation of Ferroptosis Occurs in an ACSL4-Dependent Manner in Diabetic Cardiomyopathy.Cardiovascular toxicology · 2025Article
- Baicalin affects the progression of diabetic retinopathy through the RAGE/PXDN/PI3K/AKT pathway.Journal of translational medicine · 2025Article
- A Human Engineered Heart Tissue-Derived Lipotoxic Diabetic Cardiomyopathy Model Revealed Early Benefits of Empagliflozin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bioengineering Approaches to In Vitro Modeling of Genetic and Acquired Cardiac Diseases.Current cardiology reports · 2025Review
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Of cells and tissues: Identifying the elements of a diabetic cardiac in vitro study model.Research square · 2024Article
- Neuregulin-4 protects cardiomyocytes against high-glucose-induced ferroptosis via the AMPK/NRF2 signalling pathway.Biology direct · 2024Article
- Architecture design and advanced manufacturing of heart-on-a-chip: scaffolds, stimulation and sensors.Microsystems & nanoengineering · 2024Review
- Modelling Diabetic Cardiomyopathy: Using Human Stem Cell-Derived Cardiomyocytes to Complement Animal Models.Metabolites · 2022Review
- Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022Review
- Ferroptosis is essential for diabetic cardiomyopathy and is prevented by sulforaphaneActa pharmaceutica Sinica. B · 2022Article
- Pathophysiology of RAGE in inflammatory diseases.Frontiers in immunology · 2022Review
- lncRNA ADAMTS9-AS1/circFN1 Competitively Binds to miR-206 to Elevate the Expression of ACTB, Thus Inducing Hypertrophic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Article
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Therapeutic potential of targeting oxidative stress in diabetic cardiomyopathy.Free radical biology & medicine · 2021Review
- Toxicity of advanced glycation end products (Review).Biomedical reports · 2021Review
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rodent diabetic models, used to understand the pathophysiology of diabetic cardiomyopathy (DCM), remain several limitations. Engineered cardiac tissues (ECTs) have emerged as robust 3D in vitro models to investigate structure-function relationships as well as cardiac injury and repair. Advanced glycation end-products (AGEs), produced through glycation of proteins or lipids in response to hyperglycemia, are important pathogenic factor for the development of DCM. In the current study, we developed a murine-based ECT model to investigate cardiac injury produced by AGEs. We treated ECTs composed of neonatal murine cardiac cells with AGEs and observed AGE-related functional, cellular, and molecular alterations: (1) AGEs (150 µg/mL) did not cause acute cytotoxicity, which displayed as necrosis detected by medium LDH release or apoptosis detected by cleaved caspase 3 and TUNEL staining, but negatively impacted ECT function on treatment day 9; (2) AGEs treatment significantly increased the markers of fibrosis (TGF-β, α-SMA, Ctgf, Collagen I-α1, Collagen III-α1, and Fn1) and hypertrophy (Nppa and Myh7); (3) AGEs treatment significantly increased ECT oxidative stress markers (3-NT, 4-HNE, HO-1, CAT, and SOD2) and inflammation response markers (PAI-1, TNF-α, NF-κB, and ICAM-1); and (4) AGE-induced pathogenic responses were all attenuated by pre-application of AGE receptor antagonist FPS-ZM1 (20 µM) or the antioxidant glutathione precursor N-acetylcysteine (5 mM). Therefore, AGEs-treated murine ECTs recapitulate the key features of DCM's functional, cellular and molecular pathogenesis, and may serve as a robust in vitro model to investigate cellular structure-function relationships, signaling pathways relevant to DCM and pharmaceutical intervention strategies.
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