Article in BioMed research international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
7 authors.
Lin-Xiang HuangPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0001-5140-6148
Zi-Long WangPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0003-0983-467X
Xiao-Xiao WangPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0003-1654-7302
Zi-Xuan QiuPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0009-0009-6460-398X
Jia-Rui ZhengPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0003-0202-7488
Rui JinPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0002-9051-6187
Bo FengPeking University Hepatology Institute, Infectious Disease and Hepatology Center of Peking University People's Hospital, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing International Cooperation Base for Science and Technology on NAFLD Diagnosis, Peking University People's Hospital, Beijing, China, pku.edu.cn.ORCID https://orcid.org/0000-0001-5084-6715
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Background and Aims: Primary biliary cholangitis (PBC) is an autoimmune intrahepatic cholestatic disease with both environmental and genetic participation. In this study, we aim to investigate the involvement of pyroptosis in PBC mice based on prior bioinformatic analysis of PBC patients and explore the immune cell populations potentially involved. Methods: KEGG pathway enrichment analysis was performed using the GSE119600 dataset from the Gene Expression Omnibus (GEO) database, which includes whole-blood samples from PBC patients ( Results: Toll-like receptor and NOD-like receptor signaling pathways were identified in blood samples of PBC patients in KEGG pathway enrichment analysis. In the PBC mouse model, the pyroptosis pathway was found to be upregulated by qRT-PCR ( Conclusions: Pyroptosis plays a key role in PBC patients and 2OA-BSA induced PBC mice, with macrophages possibly serving as important executors. Inhibition of the pyroptosis pathway might be a potential target for the future treatment of PBC.
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.