Department of Pharmacology, School of Pharmacy, Xinjiang Medical University, Urumqi, China.
Xinjiang Key Laboratory of Biopharmaceuticals and Medical Devices, Urumqi, China.
J Transl Med. 2024 Sep 12;22(1):839. doi: 10.1186/s12967-024-05624-7.
Myocardial fibrosis, a hallmark of heart disease, is closely associated with macrophages, yet the genetic pathophysiology remains incompletely understood. In this study, we utilized integrated single-cell transcriptomics and bulk RNA-seq analysis to investigate the relationship between macrophages and myocardial fibrosis across omics integration.
We examined and curated existing single-cell data from dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), myocardial infarction (MI), and heart failure (HF), and analyzed the integrated data using cell communication, transcription factor identification, high dimensional weighted gene co-expression network analysis (hdWGCNA), and functional enrichment to elucidate the drivers of macrophage polarization and the macrophage-to-myofibroblast transition (MMT). Additionally, we assessed the accuracy of single-cell data from the perspective of driving factors, cell typing, anti-fibrosis performance of left ventricular assist device (LVAD). Candidate drugs were screened using L1000FWD.
All four heart diseases exhibit myocardial fibrosis, with only MI showing an increase in macrophage proportions. Macrophages participate in myocardial fibrosis through various fibrogenic molecules, especially evident in DCM and MI. Abnormal RNA metabolism and dysregulated transcription are significant drivers of macrophage-mediated fibrosis. Furthermore, profibrotic macrophages exhibit M1 polarization and increased MMT. In HF patients, those responding to LVAD therapy showed a significant decrease in driver gene expression, M1 polarization, and MMT. Drug repurposing identified cinobufagin as a potential therapeutic agent.
Using integrated single-cell transcriptomics, we identified the drivers of macrophage-mediated myocardial fibrosis in four heart diseases and confirmed the therapeutic effect of LVAD on improving HF with single-cell accuracy, providing novel insights into the diagnosis and treatment of myocardial fibrosis.
心肌纤维化是心脏病的一个标志,与巨噬细胞密切相关,但遗传病理生理学仍不完全清楚。在这项研究中,我们利用整合的单细胞转录组学和批量 RNA-seq 分析来研究巨噬细胞与心肌纤维化之间的关系,通过组学整合进行分析。
我们检查和整理了来自扩张型心肌病(DCM)、缺血性心肌病(ICM)、心肌梗死(MI)和心力衰竭(HF)的现有单细胞数据,并使用细胞通讯、转录因子鉴定、高维加权基因共表达网络分析(hdWGCNA)和功能富集来分析整合数据,以阐明巨噬细胞极化和巨噬细胞向肌成纤维细胞转化(MMT)的驱动因素。此外,我们从驱动因素、细胞分型、左心室辅助装置(LVAD)抗纤维化性能的角度评估了单细胞数据的准确性。使用 L1000FWD 筛选候选药物。
所有四种心脏病都表现出心肌纤维化,只有 MI 显示巨噬细胞比例增加。巨噬细胞通过各种成纤维分子参与心肌纤维化,在 DCM 和 MI 中尤为明显。异常的 RNA 代谢和转录失调是巨噬细胞介导纤维化的重要驱动因素。此外,促纤维化巨噬细胞表现出 M1 极化和增加的 MMT。在 HF 患者中,那些对 LVAD 治疗有反应的患者表现出驱动基因表达、M1 极化和 MMT 的显著下降。药物再利用确定华蟾素作为一种潜在的治疗药物。
使用整合的单细胞转录组学,我们确定了四种心脏病中巨噬细胞介导的心肌纤维化的驱动因素,并证实了 LVAD 对改善 HF 的治疗效果具有单细胞准确性,为心肌纤维化的诊断和治疗提供了新的见解。