ArticleFrontiers in immunology2026
Yizong Tongluo formula attenuates idiopathic pulmonary fibrosis and inflammatory injury by inhibiting HIF-1α/LSH/SCD1-mediated ferroptosis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by chronic inflammation, aberrant tissue remodeling, and hypoxia. In traditional Chinese medicine (TCM), it is classified as Qi deficiency-blood stasis syndrome. The mechanism of Yizong Tongluo Formula (YZTLF), a Traditional Chinese Medicine (TCM) herbal formulation and effective pharmaceutical agent for the clinical treatment of IPF, remains unclear. Methods: This study investigated the immunomodulatory and anti-fibrotic mechanisms of YZTLF for this IPF subtype by focusing on the HIF-1α/LSH/SCD1 signaling pathway and ferroptosis-induced inflammatory injury. We began by analyzing clinical samples from IPF patients with Qi deficiency and blood stasis was conducted to assess the signalling axis and ferroptosis markers. Molecular and histological analyzes were performed using TGF-β-treated MRC-5 fibroblast cells and a bleomycin-induced rat model of pulmonary fibrosis. Results: Clinical analysis revealed a dysregulation of the HIF-1α/LSH/SCD1 axis and altered levels of ferroptosis markers in patients. Conclusion: These findings indicate that YZTLF mitigates IPF progression in the context of Qi deficiency and blood stasis by suppressing ferroptosis-driven inflammation and remodeling the hypoxic microenvironment via the HIF-1α/LSH/SCD1 pathway. This provides a mechanism-based rationale for its use in this TCM-defined IPF subtype.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.