Correlation Between "Pathological Accumulation from Collateral Obstruction" and Gap Junction Communication Dysfunction and Its Application in Tumor Prevention and Treatment
10.13288/j.11-2166/r.2025.13.002
- VernacularTitle:“络息成积”与缝隙连接细胞间通讯异常的相关性及其在肿瘤防治中的应用
- Author:
Hongtai XIONG
1
;
Ying SONG
1
;
Yanyuan DU
1
;
Peiyi YU
2
;
Honggang ZHENG
1
Author Information
1. Guang'anmen Hospital，China Academy of Chinese Medical Sciences，Beijing，100053
2. Heilongjiang Academy of Chinese Medicine
- Publication Type:Journal Article
- Keywords:
tumor microenvironment;
collaterals;
pathological accumulation from collateral obstruction;
gap junction intercellular communication
- From:
Journal of Traditional Chinese Medicine
2025;66(13):1311-1316
- CountryChina
- Language:Chinese
-
Abstract:
By reviewing modern research and integrating clinical practice， this paper elucidates the correlation between the traditional Chinese medicine theory of pathological accumulation from collateral obstruction and gap junction intercellular communication （GJIC）， as well as its theoretical connotation and clinical application in tumor prevention and treatment. Physiologically， gap junction and collateral channels share similarities in structural distribution， substance exchange and information transmission. Pathologically， metabolic coupling mediated by dysfunctional gap junction resembles collaterals stagnation， forming the basis of tumor pathogenesis. The establishment of heterotypic gap junction parallels collateral hyperactivity， contributing to tumor metastasis. The post-translational modifications （PTMs） disorder of connexins is similar to the deficiency of collaterals， serving as a driver of tumor progression. Clinically， tumor treatment should follow the pathomechanism of collateral obstruction leading to pathological accumulation. In the early stage， detoxifying and unblocking collaterals can restore intercellular communication and inhibit tumorigenesis； in the progressive stage， calming hyperactivity and suppressing aberrant collateral pathways can prevent metastasis by interrupting heterotypic gap junction formation； and in the terminal stage， supporting vital qi and modulating PTMs of connexins can help delay tumor progression.
