Pathogenetic Interpretation and Differentiation and Treatment Strategies for Gasdermin D-Mediated Pyroptotic Microenvironmental Imbalance in Colorectal Cancer：from the Perspective of the Cancer-Toxin Pathogenesis Theory
10.13288/j.11-2166/r.2026.19.006
- VernacularTitle:癌毒病机理论视角下结直肠癌消皮素D介导焦亡微环境失衡的病机阐释及辨治思路
- Author:
Gehui XU
1
;
Xiaohe SUN
1
;
Liu LI
1
;
Haibo CHENG
1
Author Information
1. The First School of Clinical Medicine，Nanjing University of Chinese Medicine，Nanjing，210023
- Publication Type:Journal Article
- Keywords:
colorectal cancer;
cancer-toxin;
pathogenesis;
spleen qi depletion;
damp heat and stasis toxin;
gasdermin D;
cell pyroptosis;
tumor microenvironment
- From:
Journal of Traditional Chinese Medicine
2026;67(19):2063-2067
- CountryChina
- Language:Chinese
-
Abstract:
Based on the theory of cancer-toxin pathogenesis， this article proposes that cancer toxin persists throughout the entire course of colorectal cancer （CRC）， with spleen qi depletion as the root of disease and damp-heat and stasis toxin as key factors in the evolution of pathogenesis. It further explores the intrinsic relationship between these pathogenetic features and the modern pathological process of "inflammasome pre-activation/repeated activation/gasdermin D-mediated pyroptotic microenvironmental imbalance". Spleen qi depletion is regarded as an upstream pathological basis for inflammasome pre-activation， while damp-heat and stasis toxin are considered key drivers of repeated inflammasome activation， the gasdermin D-mediated amplification of pyroptotic inflammation， and persistent microenvironmental imbalance. These two pathogenetic aspects interact sequentially and concurrently， jointly contributing to the early development and progression of CRC. Guided by the principle of anti-cancer and detoxification， and based on the traditional Chinese medicine （TCM） treatment strategy of simultaneously fortifying the spleen and replenishing qi， clearing and resolving damp-heat， and resolving stasis and toxins， this study further elucidates the modern mechanistic connotations of how these relevant therapies intervene in the gasdermin D-mediated pyroptotic microenvironment imbalance in CRC. The ultimate aim is to provide a theoretical basis for the modern scientific interpretation of cancer-toxin pathogenesis and the clinical syndrome differentiation and treatment of CRC.
