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Advancing cardiac tissue engineering requires innovative fabrication techniques, including 3D bioprinting and tissue maturation, to enable the generation of new muscle for repairing or replacing damaged heart tissue. Recent advances in tissue engineering have highlighted the need for rapid, high-resolution bioprinting methods that preserve cell viability and maintain structural fidelity. Traditional collagen-based bioinks gel slowly, limiting their use in bioprinting. Here, we implement TRACE (tunable rapid assembly of collagenous elements), a macromolecular crowding-driven bioprinting technique that enables the immediate gelation of collagen bioinks infused with cells. This overcomes the need for extended incubation, allowing for direct bioprinting of engineered cardiac tissues with high fidelity. Unlike methods that rely on high-concentration acidic collagen or fibrin for gelation, TRACE achieves rapid bioink stabilization without altering the biochemical composition. This ensures greater versatility in bioink selection while maintaining functional tissue outcomes. Additionally, agarose slurry provides stable structural support, preventing tissue collapse while allowing nutrient diffusion. This approach better preserves complex tissue geometries during culture than gelatin-based support baths or polydimethylsiloxane (PDMS) molds. Our results demonstrate that TRACE enables the bioprinting of structurally stable cardiac tissues with high resolution. By supporting the fabrication of biomimetic tissues, TRACE represents a promising advancement in bioprinting cardiac models and other engineered tissues.
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http://dx.doi.org/10.1063/5.0252746 | DOI Listing |
Pathol Res Pract
September 2025
Adiyaman University, Faculty of Medicine, Department of Anesthesiology and Reanimation, Adiyaman, Turkey. Electronic address:
Aim: This study aims to evaluate the effects of bupivacaine on acute kidney injury (AKI) through kidney function parameters and cardiac tissue damage via TRPM2, HSP70, TLR4, NF-κB, and TNF-α biomarkers.
Material And Method: Male Wistar albino rats were divided into 4 groups, with seven rats in each group: Control group, AKI group (kidney damage induced by glycerol), AKI + L group (group treated with bupivacaine), and L group (group treated with bupivacaine alone). At the end of the experiment, kidney and heart tissues were collected for histological analysis, and serum samples were taken for biochemical analysis.
Expert Opin Investig Drugs
September 2025
Heart Failure Clinic, Division of Cardiology, Alessandro Manzoni Hospital, ASST Lecco, Lecco, Italy.
Introduction: Ischemic heart disease (IHD) constitutes the most prevalent form of cardiac disease in the general population. Although current therapeutic interventions have significantly improved both quality of life and survival rates, no available treatment can reverse the loss of cardiomyocytes resulting from ischemic injury. Existing therapies are limited to attenuating myocardial damage, reducing its extent, and mitigating its clinical consequences.
View Article and Find Full Text PDFJ Mol Cell Cardiol
September 2025
Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Selective therapeutic targeting of cardiomyocytes (CMs) and non-myocytes (NMs) within the heart is an active field of research. The success of those novel therapeutic strategies is linked to the ability to accurately assess uptake and gene delivery efficiencies in clinically relevant animal models. Nevertheless, quantification at the single cell level remains a significant challenge.
View Article and Find Full Text PDFBiomaterials
August 2025
Department of Anesthesiology and Perioperative Medicine, The Second Affiliated Hospital of Anhui Medical University, 678 Furong Road, Hefei, 230601, China; Key Laboratory of Anesthesiology and Perioperative Medicine of Anhui Higher Education Institutes, Anhui Medical University, 678 Furong Road, Hef
Activation of p38 mitogen-activated protein kinase plays an important role in the progression of ventricular muscle inflammation after myocardial ischemia-reperfusion (MI/R). The inhibition of p38 activation in ischemic myocardium can reduce ventricular muscle remodeling post-MI. However, owing to the dynamic change of p38 in ischemic myocardium after MI, the clinical therapeutic effect of p38 inhibitors is insufficient.
View Article and Find Full Text PDFAtherosclerosis
August 2025
Institute for Clinical Chemistry and Laboratory Medicine, UniversityHospital and Faculty of Medicine, TU Dresden, 01307, Dresden, Germany; National Center for Tumor Diseases, Partner Site Dresden, 01307, Dresden, Germany; Paul Langerhans Institute Dresden of the Helmholtz Center Munich, University
Due to their remarkable plasticity, macrophages can adapt to diverse environments and challenges therein, thereby exerting tissue-specific and context-specific functions. Macrophages are the most frequent immune cell population present in the heart and contribute substantially to cardiac homeostasis and function. Moreover, macrophages are key regulators throughout all stages of heart injury, acquiring diverse phenotypes that can either ameliorate or exacerbate cardiac pathology in a context-dependent manner.
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