心肌梗死患者心内血管血管周围纤维化和前纤维化细胞转变增加。

Journal of molecular and cellular cardiology plus Pub Date : 2024-12-01 DOI:10.1016/j.jmccpl.2024.100275

Zhu Jiang , Giulia Sorrentino , Suat Simsek , Joris J.T.H. Roelofs , Hans W.M. Niessen , Paul A.J. Krijnen

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引用次数: 0

摘要

背景和目的：心肌微循环的结构和功能改变增加心肌梗死（MI）的风险。本研究通过对急性和亚急性心肌梗死死亡患者心肌内血管周围纤维化和前纤维化细胞转移的研究，探讨其在心肌梗死发病机制中的作用。方法：在心肌梗死急性期(3 ~ 6 h；n = 24)，亚急性期MI(5-14天；N = 12)和非梗死对照组（N = 14）。采用免疫组化方法定量测定血管周围纤维化和成纤维细胞活化蛋白（FAP）的表达。应用免疫荧光显微镜定量观察血管平滑肌细胞（VSMC）和内皮细胞（EC）的成纤维样转化。结果：心肌梗死急性期（77.69%）和亚急性期（72.19%：交界区95.18%：梗死核心）患者血管周围纤维化升高（p p p p）。结论：心肌梗死患者心肌血管血管周围纤维化、成纤维细胞活化和血管细胞转化的增加可能与心肌梗死的发展有关。FAP表达和血管周围纤维化的进一步增加，特别是在亚急性期梗死核心，表明心肌梗死本身加剧了成纤维细胞活化和血管周围纤维化，理论上增加了再梗死的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Increased perivascular fibrosis and pro-fibrotic cellular transition in intramyocardial blood vessels in myocardial infarction patients

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Increased perivascular fibrosis and pro-fibrotic cellular transition in intramyocardial blood vessels in myocardial infarction patients

Background and objectives

Structural and functional changes in the intramyocardial microcirculation increase the risk of myocardial infarction (MI). This study investigated intramyocardial perivascular fibrosis and pro-fibrotic cellular transitions in deceased acute and subacute MI patients to explore their involvement in the pathogenesis of MI.

Methods

Left ventricular tissue (LV) was obtained from the infarction area of autopsied patients with acute-phase MI (3–6 h; n = 24), subacute-phase MI (5–14 days; n = 12), and noninfarcted controls (n = 14). Perivascular fibrosis and fibroblast activation protein (FAP) expression were quantified using (immuno)histochemistry. Fibroblast-like transitioning of vascular smooth muscle cells (VSMC) and endothelial cells (EC) was quantified using immunofluorescent microscopy.

Results

Perivascular fibrosis was elevated in acute-phase (77.69 %) and subacute-phase (72.19 %: border zone 95.18 %: infarct core) MI patients (p < 0.0001) compared to controls (61.03 %). FAP expression was higher in both acute-phase (1.46 %) and subacute-phase (18.01 %: border zone 5.67 %: infarct core) compared to controls (0.46 %) (p < 0.05). VSMC fibroblast-like cellular transition (SMA + S100A4+ vessels fraction) was higher in acute-phase (31.96 %) and subacute-phase (21.90 %: border zone; 37.25 %: infarct core) MI compared to controls (8.95 %) (p < 0.05). Similarly, EC fibroblast-like cellular transition (CD31 + S100A4+ area fraction) was increased in acute-phase MI (10.14 %) and subacute-phase MI (8.31 %: border zone 10.15 %: infarct core) compared to controls (2.67 %) (p < 0.05).

Conclusion

Increased perivascular fibrosis, fibroblast activation and vascular cellular transition in intramyocardial blood vessels of MI patients may contribute to MI development. Further increases of FAP expression and perivascular fibrosis, particularly in subacute-phase infarct cores, suggest MI itself exacerbates fibroblast activation and perivascular fibrosis, theoretically increasing reinfarction risk.

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来源期刊

Journal of molecular and cellular cardiology plus Cardiology and Cardiovascular Medicine

自引率

0.00%

发文量

审稿时长

31 days