3D Bioprinted Fat-Myocardium Model Unravels the Role of Adipocyte Hypertrophy in Atrial Dysfunction.
Celebi LE., Zorlutuna P.
Animal Study on Type 2 Diabetes, Cardiovascular Disease, published in Adv Sci (Weinh) (2026) — summary generated from the PubMed abstract.
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Adv Sci (Weinh) (2026)
- Country
- Germany
- Reported sample size
- —
- PMID
- 41655215
- DOI
- 10.1002/advs.202516114
Abstract (original English)
Cardiovascular diseases (CVD) are the leading cause of mortality in individuals with obesity. Epicardial adipose tissue (EAT) dysfunction serves as a link between obesity and CVD, promoting inflammatory and metabolic alterations that increase CVD risk. While EAT normally supports cardiac health, obesity-induced adipocyte hypertrophy triggers excessive fatty acid and cytokine release, driving myocardial lipotoxicity and inflammation that impair electrophysiology and metabolism, leading to beating irregularities, insulin resistance, and heart failure. The lack of sufficient EAT in small animal models and the impracticality of using large mammals hinder insights into the effects of EAT hypertrophy on the myocardium. To address this gap, a human-derived 3D bioprinted coculture of obese adipocytes and cardiomyocytes (CMs) is developed using patient-derived adipocytes and human induced pluripotent stem cell (hiPSC)-derived atrial CMs (a-iCMs). This platform enables the investigation of both cell-cell and paracrine interactions between hypertrophic adipocytes and a-iCMs, allowing assessment of electrophysiological, structural, and proteomic changes to uncover mechanisms linking EAT hypertrophy to obesity-related atrial dysfunction. Screening of metformin, a cardioprotective drug, reveals improvement in electrophysiological function in hypertrophic adipocyte-a-iCM cocultures. 3D biopri
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence comes from animal or laboratory studies and has not been confirmed in humans.
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