Long non-coding RNA predicting cardiac remodeling (lnc LIPCAR) was implicated in several human diseases, while its role in atrial fibrillation (AF) remained poorly understood. Our study aimed to discover the role of LICPAR played in AF.

Samples of atrial muscle tissues from patients diagnosed with sinus rhythm (SR) and atrial fibrillation (AF) were collected, and human atrial fibroblasts were isolated and identified under immunofluorescence staining. After Angiotensin II (Ang II, as a activator of TGF-β) stimulation with LICPAR overexpression or knockdown, the viability and proliferation of atrial fibroblasts were respectively determined using cell counting kit-8 (CCK-8) assay and clone formation assay. Relative expressions of LICPAR, fibrosis- and transforming growth factor-β (TGF-β)/Smad2/3-pathway related proteins were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed.

LICPAR and TGF-β1 were upregulated and were positively correlated in atrial muscle tissues from AF. Atrial fibroblasts were identified as Vimentin positive. Further analysis indicated that Ang II enhanced the levels of LIPCAR, Smad2/3 phosphorylation and α-smooth muscle actin (α-SMA). Also, upregulating LIPCAR further promoted the promotive effects of Ang II on levels of LIPCAR, Collagen I, Collagen II, α-SMA and Smad2/3 phosphorylation, cell viability and proliferation of atrial fibroblasts, whereas silencing LIPCAR resulted in opposite effects.

LICPAR regulates atrial fibrosis via modulating TGF-β/Smad pathway, which provided a potential therapeutic method for AF in clinical practice in the future.

预测心脏重构的长链非编码 RNA (lnc LIPCAR) 与多种人类疾病有关，而其在心房颤动 (AF) 中的作用仍知之甚少。我们的研究旨在发现 LICPAR 在 AF 中的作用。

收集诊断为窦性心律 (SR) 和心房颤动 (AF) 的患者的心房肌肉组织样本，并在免疫荧光染色下分离和鉴定人心房成纤维细胞。在血管紧张素 II（Ang II，作为 TGF-β 的激活剂）用 LICPAR 过表达或敲低刺激后，使用细胞计数试剂盒-8（CCK-8）测定和克隆形成测定分别测定心房成纤维细胞的活力和增殖。根据需要使用定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹测量 LICPAR、纤维化和转化生长因子-β (TGF-β)/Smad2/3-通路相关蛋白的相对表达。

LICPAR 和 TGF-β1 在 AF 的心房肌肉组织中上调并呈正相关。心房成纤维细胞被鉴定为波形蛋白阳性。进一步分析表明，Ang II 提高了 LIPCAR、Smad2/3 磷酸化和 α-平滑肌肌动蛋白 (α-SMA) 的水平。此外，上调 LIPCAR 进一步促进了 Ang II 对 LIPCAR、胶原蛋白 I、胶原蛋白 II、α-SMA 和 Smad2/3 磷酸化水平、细胞活力和心房成纤维细胞增殖的促进作用，而沉默 LIPCAR 导致相反的效果。

LICPAR 通过调节 TGF-β/Smad 通路调节心房纤维化，为未来临床实践中 AF 提供了一种潜在的治疗方法。