ArticleFrontiers in pharmacology2026
The biological basis of Blood-Heat syndrome in children with Henoch-Schonlein purpura nephritis: a multidimensional analysis based on clinical proteomics and an animal model.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
Objective: Blood-Heat syndrome is a core syndrome of Traditional Chinese Medicine (TCM) in Henoch-Schönlein purpura nephritis (HSPN), yet its biological basis remains unclear. This study aimed to systematically elucidate the scientific basis of Blood-Heat syndrome within the context of HSPN and to identify its objective biomarkers using a multidimensional biological approach. Methods: In the clinical research part, we divided it into a discovery cohort and a validation cohort. The discovery cohort employed Data-Independent Acquisition (DIA) proteomics technology to analyze serum samples from HSPN patients with Blood-Heat syndrome (n = 15), those without Blood-Heat syndrome (non-Blood-Heat, n = 30), and healthy controls (n = 30). The findings were then validated through ELISA in both the discovery cohort and an independent validation cohort (n = 30 for blood heat syndrome, n = 30 for non-blood heat syndrome). In the basic research component, we established a rat model combining HSPN with Blood-Heat syndrome to replicate the clinical findings. Results: Proteomic analysis identified 87 specific differentially expressed proteins (DEPs) associated with Blood-Heat syndrome. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed significant enrichment in the sphingolipid signaling pathway ( Conclusion: Based on multidimensional evidence from clinical proteomics and animal model replication, this study suggests that Blood-Heat syndrome in the context of HSPN has a reproducible molecular phenotype. The functional enrichment of its differential proteins involves the sphingolipid signaling pathway, accompanied by an enhanced inflammatory background represented by ERK2 upregulation. Based on these findings, we propose a core scientific hypothesis of "Blood-Heat-related stress-sphingolipid signaling-associated alterations-ERK2-mediated inflammatory amplification," providing a direction for future mechanistic validation and targeted intervention research.
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