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1.北京中医药大学 东直门医院,北京 100700
2.北京中医药大学,北京 100029
Received:22 August 2024,
Accepted:01 November 2024,
Published Online:05 November 2024,
Published:20 March 2025
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滕俊,李磊,夏君彦等.病络视域下气管支气管腺样囊性癌血管招募探赜[J].中国实验方剂学杂志,2025,31(06):260-269.
TENG Jun,LI Lei,XIA Junyan,et al.Exploring Vascular Recruitment in Tracheobronchial Adenoid Cystic Carcinoma from Perspective of Abnormal Collateral[J].Chinese Journal of Experimental Traditional Medical Formulae,2025,31(06):260-269.
滕俊,李磊,夏君彦等.病络视域下气管支气管腺样囊性癌血管招募探赜[J].中国实验方剂学杂志,2025,31(06):260-269. DOI: 10.13422/j.cnki.syfjx.20250693.
TENG Jun,LI Lei,XIA Junyan,et al.Exploring Vascular Recruitment in Tracheobronchial Adenoid Cystic Carcinoma from Perspective of Abnormal Collateral[J].Chinese Journal of Experimental Traditional Medical Formulae,2025,31(06):260-269. DOI: 10.13422/j.cnki.syfjx.20250693.
气管支气管腺样囊性癌(TACC)是一种源自气道黏膜的低度恶性肿瘤,虽进展缓慢,但具备高侵袭性、易复发和高转移的特性。临床前研究表明血管靶向治疗潜力较大,但针对TACC的有效全身治疗方案尚未确立。该文以中医肺积范畴下的TACC为切入点,深入探讨了病络与肿瘤血管招募的机制,并进一步阐释了病络与肿瘤血管招募理蕴相通。首先,络道亢变导致肺络纵横错杂、布列失序,其异常结构与肿瘤(类)血管新生的无序迂曲相似,致使肺络的流通、渗灌及反注功能失衡,进而引发络道恣行不羁、诸邪搏结成积;其次,TACC中细胞外基质(ECM)重塑和上皮-间充质转化(EMT)作为血管共择(VCO)发生的关键环节,是营卫倾移在微观层面的体现。此过程中,ECM重塑与EMT促使TACC细胞更易劫持正常血管,形成复杂且有利于肿瘤生长的血管微环境。治疗方面,该文提出“通络祛邪、荣络养正”的中医策略,并列举潜在中药,通过调节络脉气血、修复病络功能,干预TACC的血管招募过程。未来研究应聚焦于完善TACC的中医临床证候学特征,并借助现代分子生物学技术,深入解析TACC血管招募的微观图谱,丰富病络与肿瘤血管招募的幽契之意,为中医药靶向血管招募治疗TACC提供实证依据。
Tracheobronchial adenoid cystic carcinoma (TACC) is a low-grade malignant tumor originating from the airway mucosa. Despite its slow progression,it is characterized by high invasiveness,frequent recurrence,and a strong tendency for metastasis. Preclinical studies have shown that vascular-targeted therapy holds significant potential. However,an effective systemic treatment for TACC has not been established yet. This study explored TACC from the perspective of "Feiji" in traditional Chinese medicine (TCM) as the starting point. It deeply investigated the mechanisms of abnormal collaterals and tumor vascular recruitment and further elaborated on the theoretical connection between abnormal collaterals and tumor vascular recruitment. Firstly,collateral hyperactivity led to disordered and erratic pulmonary collaterals. Their abnormal structures were similar to the disorderly and tortuous nature of tumor (pseudo)angiogenesis. This resulted in imbalances in the functions of circulation,perfusion,and reverse injection of the pulmonary collaterals,and then led to unrestrained collateral dysfunction and the accumulation of pathogenic factors. Secondly,the remodeling of the extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT) in TACC were critical processes in vascular co-option (VCO),representing the micro-level manifestation of the displacement of nutrient and defense. During this process,ECM remodeling made TACC cells more likely to hijack normal blood vessels,creating a complex vascular microenvironment conducive to tumor growth. In terms of treatment,this study proposed a TCM strategy of "regulating collaterals to expel pathogenic factors and nourishing collaterals to strengthen the healthy Qi",and listed potential TCM. These were intended to regulate the Qi and blood in the collaterals,repair the functions of abnormal collaterals,and intervene in the vascular recruitment process of TACC. Future research should focus on improving the TCM clinical syndrome characteristics of TACC. Through modern molecular biology techniques,it is necessary to deeply analyze the micro-level pattern of vascular recruitment in TACC. This would enrich the understanding of the profound connection between abnormal collaterals and tumor vascular recruitment,providing empirical evidence for TCM-targeted therapies for vascular recruitment in TACC.
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