心肌纤维化是心力衰竭等心血管疾病演化过程中的关键性病理改变，该病的进展机制依赖巨噬细胞与成纤维细胞的相互调控。现有现代医学研究证实巨噬细胞可凭借M1、M2表型极化行为介导炎症反应与组织修复过程，成纤维细胞能够分化形成肌成纤维细胞并推动细胞外基质异常沉积，两类细胞可依托TGF-β/Smad、CSF-1/CSF-1R等信号通路构建相互调控的作用网络并介导心肌纤维化恶化。中医痰瘀互结病机理论指出痰浊与瘀血可相互滋生、交织阻滞，是各类慢性迁延性疾病的关键发病基础。本文以中医痰瘀互结理论为研究切入点，剖析该病机理论与巨噬细胞、成纤维细胞交互作用的内在关联，整合现代医学关于两种细胞交互作用的现有研究成果，深入分析细胞互作在心肌纤维化发病过程中的协同机制与病理关联，旨在为心肌纤维化的中西医协同防治提供理论依据，为相关动物实验及临床应用研究筑牢研究基础。

Myocardial fibrosis is a key pathological change in the progression of cardiovascular diseases such as heart failure. The progression mechanism of this disease relies on the reciprocal regulation between macrophages and fibroblasts. Current modern medical research has confirmed that macrophages can mediate inflammatory responses and tissue repair processes through M1 and M2 phenotypic polarization behaviors, and fibroblasts can differentiate into myofibroblasts and promote abnormal extracellular matrix deposition. The two types of cells can construct a reciprocal regulatory network through signaling pathways such as TGF-β/Smad and CSF-1/CSF-1R, thereby mediating the deterioration of myocardial fibrosis. The theory of phlegm and blood stasis intermingling in traditional Chinese medicine suggests that phlegm turbidity and blood stasis can mutually generate and interweave to cause obstruction, serving as a key pathological basis for various chronic and persistent diseases. This article takes the traditional Chinese medicine theory of phlegmblood stasis intermingling as a research entry point, analyzes the intrinsic relationship between this pathological theory and the interaction of macrophages and fibroblasts, integrates existing modern medical research findings on the interaction between the two cell types, and deeply analyzes the synergistic mechanisms and pathological correlations of cellcell interactions in the pathogenesis of myocardial fibrosis. The aim is to provide a theoretical basis for the integrated traditional Chinese and Western medicine prevention and treatment of myocardial fibrosis, and also to lay a solid research foundation for related animal experiments and clinical application studies.

心肌纤维化是心力衰竭等心血管疾病演化过程中的关键性病理改变，该病的进展机制依赖巨噬细胞与成纤维细胞的相互调控。现有现代医学研究证实巨噬细胞可凭借M1、M2表型极化行为介导炎症反应与组织修复过程，成纤维细胞能够分化形成肌成纤维细胞并推动细胞外基质异常沉积，两类细胞可依托TGF-β/Smad、CSF-1/CSF-1R等信号通路构建相互调控的作用网络并介导心肌纤维化恶化。中医痰瘀互结病机理论指出痰浊与瘀血可相互滋生、交织阻滞，是各类慢性迁延性疾病的关键发病基础。本文以中医痰瘀互结理论为研究切入点，剖析该病机理论与巨噬细胞、成纤维细胞交互作用的内在关联，整合现代医学关于两种细胞交互作用的现有研究成果，深入分析细胞互作在心肌纤维化发病过程中的协同机制与病理关联，旨在为心肌纤维化的中西医协同防治提供理论依据，为相关动物实验及临床应用研究筑牢研究基础。

Myocardial fibrosis is a key pathological change in the progression of cardiovascular diseases such as heart failure. The progression mechanism of this disease relies on the reciprocal regulation between macrophages and fibroblasts. Current modern medical research has confirmed that macrophages can mediate inflammatory responses and tissue repair processes through M1 and M2 phenotypic polarization behaviors, and fibroblasts can differentiate into myofibroblasts and promote abnormal extracellular matrix deposition. The two types of cells can construct a reciprocal regulatory network through signaling pathways such as TGF-β/Smad and CSF-1/CSF-1R, thereby mediating the deterioration of myocardial fibrosis. The theory of phlegm and blood stasis intermingling in traditional Chinese medicine suggests that phlegm turbidity and blood stasis can mutually generate and interweave to cause obstruction, serving as a key pathological basis for various chronic and persistent diseases. This article takes the traditional Chinese medicine theory of phlegmblood stasis intermingling as a research entry point, analyzes the intrinsic relationship between this pathological theory and the interaction of macrophages and fibroblasts, integrates existing modern medical research findings on the interaction between the two cell types, and deeply analyzes the synergistic mechanisms and pathological correlations of cellcell interactions in the pathogenesis of myocardial fibrosis. The aim is to provide a theoretical basis for the integrated traditional Chinese and Western medicine prevention and treatment of myocardial fibrosis, and also to lay a solid research foundation for related animal experiments and clinical application studies.

Wnt/β-catenin信号通路是一种在胚胎发育,细胞增殖分化、迁移,干细胞更新等中起关键作用的蛋白质家族。Wnt/β-catenin信号通路的失调常常会导致各种严重的疾病,例如肿瘤、心脏疾病、肺部疾病、肝脏疾病、骨骼疾病、神经疾病等。大量研究表明,Wnt/β-catenin信号通路在心肌纤维化发病机制中起重要作用,本文结合最新研究成果,从心肌纤维化相关疾病的角度对Wnt/β-catenin通路进行综述,为预防心肌纤维化提供新的思路,进一步达到防治心血管疾病的目的。

The Wnt/β-catenin signaling pathway is a family of proteins that play a key role in embryonic development,cell proliferation and differentiation,migration,stem cell renewal,etc．Dysfunctions of Wnt/β-catenin signaling pathway often lead to various serious diseases,such as tumor,heart,lung,liver,bone and neurological diseases,etc．Numerous studies have shown that the Wnt/β-catenin signaling pathway plays an important role in the pathogenesis of cardiac fibrosis．This article,in combination with the latest research findings,presents a review of the Wnt/β-catenin pathway from the perspective of myocardial fibrosis-related diseases,in order to provide new ideas for preventing myocardial fibrosis and achieving the goal of combating cardiovascular disease．

目的 探讨I¹³¹联合促甲状腺激素(TSH)抑制治疗对术后中高危组甲状腺乳头状癌(PTC)患者心肌纤维化及心房颤动(AF)的影响。方法 选取2016年8月—2017年8月南华大学附属第一医院收治的因PTC行甲状腺双侧腺叶全切术或近全切除术患者69例,根据复发危险度分层分为中危组(49例)和高危组(20例), 两组患者均行I¹³¹ 联合TSH抑制治疗,治疗后嘱患者3个月进行1次复诊或自觉不适及时复诊,观察患者心血管系统症状、心房颤动及心肌纤维化发生情况,患者治疗前后可溶性基质溶素-2(sST2)、生长分化因子-15(GDF-15)、半乳糖凝集素-3 (GAL-3)及血清乳酸脱氢酶(LDHA)含量变化。结果 I¹³¹联合TSH抑制治疗后患者心房颤动发生率和心肌纤维化相关指标水平明显高于治疗前,且高危组患者治疗后心房颤动发生率和心肌纤维化相关指标水平高于中危组,差异均有统计学意义(P<0.05)。结论 I¹³¹联合TSH抑制治疗会增加PTC患者心肌纤维化和心房颤动的发生概率,且高危组PTC患者心肌纤维化和房颤的发生率高于中危组。

Objective To investigate the impact of I¹³¹ combined with thyroid-stimulating hormone(TSH) for suppressive treatment on myocardial fibrosis(MF) and atrial fibrillation(AF) in patients with papillary thyroid (PTC). Methods 69 patients with PTC undergoing total or subtotal thyroidectomy admitted into First Affiliated Hospital of University of South China from Aug. 2016 to Aug. 2017 were selected and divided into middle-risk group (49 cases) and high-risk group (20 cases) according to the recurrence risk stratification. Two groups of patients were given I¹³¹ combined with thyroid-stimulating hormone for suppressive treatment. The patients were instructed to undergo a follow-up visit every 3 months after treatment or whenever felt unwell. The incidences of cardiovascular system symptoms, atrial fibrillation and myocardial fibrosis, changes of contents of serum soluble ST2 (sST2), growth differentiation factor-15 (GDF-15), galectin-3 (GAL-3) and lactate dehydrogenase A (LDHA) were observed. Results After I¹³¹ combined with thyroid-stimulating hormone suppressive treatment, the incidences of atrial fibrillation and myocardial fibrosis after treatment were higher than that before treatment, and the incidences of atrial fibrillation and myocardial fibrosis of high-risk group were higher than those of the middle-risk group, with statistically significant differences (P＜0.05). Conclusion Combined use of I¹³¹ and thyroid-stimulating hormone for suppressive treatment can increase the incidences of atrial fibrillation and ventricular remodeling of patients with PTC, and the incidences of high-risk group were higher than those of the middle-risk group.