Jang Yongjun, Kang Myeongjin, Kang Yong Guk, Lee Dongtak, Jung Hyo Gi, Yoon Dae Sung, Kim Jongseong, Park Yongdoo
Department of Biomedical Sciences, College of Medicine, Korea University, Seoul, Republic of Korea.
School of Biomedical Engineering, Korea University, Seoul, Republic of Korea.
J Tissue Eng. 2025 Aug 21;16:20417314251356321. doi: 10.1177/20417314251356321. eCollection 2025 Jan-Dec.
Cardiac fibroblasts play an important role in heart homeostasis, regeneration, and disease by producing extracellular matrix (ECM) proteins and remodeling enzymes. Under normal conditions, fibroblasts exist in a quiescent state and maintain homeostasis, such as tissue structure and ECM turnover. However, if they become activated upon stimuli, such as injury, aging, or mechanical stress, which can lead to disease through excessive cell proliferation and ECM production. In addition to their role in disease progression, it remains unclear how cardiac fibroblasts contribute to cardiac maturation during development and whether the mechanism driving cytokine and ECM production during development aligns with those observed in pathological conditions. In this study, we investigated the functional and structural maturation of engineered cardiac tissue by modulating fibroblast activity within a three-dimensional (3D) in vitro model. In this model, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and human primary cardiac fibroblasts (FBs) were co-cultured in a fibrin gel and their morphology, beating characteristics, beating force, and mRNA expression profiles were analyzed. The results demonstrate that functional and structural maturation were enhanced by fibroblast-driven tissue contraction and collagen deposition, while inhibition of ECM remodeling impaired both processes. However, excessive collagen accumulation reduced functional maturation by limiting contractile efficiency. Our data suggest that ECM remodeling by cardiac fibroblasts is essential for cardiac tissue maintenance and maturation. Additionally, the regulation of collagen deposition by fibroblast activity will be a key focus of future research, as it may critically influence both cardiac development and the progression of heart disease.
心脏成纤维细胞通过产生细胞外基质(ECM)蛋白和重塑酶,在心脏稳态、再生和疾病中发挥重要作用。在正常情况下,成纤维细胞处于静止状态并维持稳态,如组织结构和ECM周转。然而,如果它们在诸如损伤、衰老或机械应力等刺激下被激活,可能会通过过度的细胞增殖和ECM产生导致疾病。除了它们在疾病进展中的作用外,目前尚不清楚心脏成纤维细胞在发育过程中如何促进心脏成熟,以及发育过程中驱动细胞因子和ECM产生的机制是否与病理条件下观察到的机制一致。在本研究中,我们通过在三维(3D)体外模型中调节成纤维细胞活性,研究了工程化心脏组织的功能和结构成熟。在该模型中,将人诱导多能干细胞衍生的心肌细胞(hiPSC-CMs)和人原代心脏成纤维细胞(FBs)在纤维蛋白凝胶中共培养,并分析它们的形态、跳动特征、搏动力和mRNA表达谱。结果表明,成纤维细胞驱动的组织收缩和胶原蛋白沉积增强了功能和结构成熟,而ECM重塑的抑制则损害了这两个过程。然而,过多的胶原蛋白积累通过限制收缩效率降低了功能成熟。我们的数据表明,心脏成纤维细胞进行的ECM重塑对于心脏组织的维持和成熟至关重要。此外,通过成纤维细胞活性调节胶原蛋白沉积将是未来研究的一个关键重点,因为它可能对心脏发育和心脏病进展都产生至关重要的影响。