Immune-Metabolic Reprogramming in Hepatic Fibrosis and Its Micro-Level Syndrome Differentiation and Treatment：from the Perspective of "Liver Being the General and Spleen Being the Defender"
10.13288/j.11-2166/r.2026.12.007
- VernacularTitle:从“肝为之将，脾为之卫”探析肝纤维化免疫-代谢重编程及其辨治策略
- Author:
Jiqi OUYANG
1
;
Yi WANG
1
;
Yaocun SHEN
1
;
Wenliang LYU
1
Author Information
1. Guang'anmen Hospital，China Academy of Chinese Medical Sciences，Beijing，100053
- Publication Type:Journal Article
- Keywords:
hepatic fibrosis;
immune imbalance;
metabolic reprogramming;
liver being the general and spleen being the defender
- From:
Journal of Traditional Chinese Medicine
2026;67(12):1277-1283
- CountryChina
- Language:Chinese
-
Abstract:
Guided by the classical theory of "the liver being the general and the spleen being the defender"， this study explores the intrinsic relationship between the pathogenesis of hepatic fibrosis （HF） and immune-metabolic reprogramming. It is proposed that the pathogenesis of HF in traditional Chinese medicine demonstrates a high degree of biological correspondence to the modern medical concept of the immune-metabolic interaction network. Specifically， immune homeostasis imbalance is analogous to the failure of the spleen's defense and malnourishment of the liver collaterals； lipid metabolic disorder and inflammatory infiltration correspond to the wood constraint， earth congestion， and phlegm-dampness turbid accumulation； "heat-transformation brewing toxin" promotes glycolytic reprogramming and， together with "healthy qi deficiency and stasis binding" leads to microenvironment deterioration. Accordingly， a micro-level syndrome differentiation and treatment strategy is proposed， which emphasizes on enriching earth and nourishing wood， consolidating defense and moistening collaterals to restore immune homeostasis， soothing the liver and activating the spleen， dispelling dampness and eliminate turbidity to correct lipid metabolic disorder， clearing heat and removing toxins， reinforcing healthy qi and resolving stasis to intervene in glycolytic reprogramming and the inflammatory microenvironment， thereby ameliorating the progression of HF.
