Evidence map›Paper›PMID 41150795›Full record

ArticleCurrent issues in molecular biology2025

Empagliflozin Attenuates Liver Inflammation and Fibrosis in NAFLD: Evidence from Mendelian Randomization and Mouse Experiments.

Chao Fu, Lijiao Deng, Xiaochan Zhu, Bin Wang, Bin Hu, Huan Xue, Qingxuan Zeng, Yi Zhang

Abstract read
In one paragraph

Article in Current issues in molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
4 · The record

Corrections and comments

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

8 authors.

Chao FuDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Lijiao DengDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.ORCID 0009-0001-4608-1454
Xiaochan ZhuDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Bin WangDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Bin HuDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Huan XueDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Qingxuan ZengDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.
Yi ZhangDepartment of Pharmacology, School of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China.ORCID 0000-0003-0305-3127

Funding

Key Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, China Key Laboratory of Cellular PhysiologyNational Natural Science Foundation of China 82404445National Natural Science Foundation of China 82404720Shanxi Province Higher Education "Billion Project" Science and Technology Guidance Project BYJL024Shanxi Province Science Foundation for Youths 202203021212363Shanxi Provincial Central Leading Local Science and Technology Development Fund Project YDZJSX20231A059Special Fund from Medicinal Basic Research Innovation Center of Chronic Kidney Disease, Ministry of Education, Shanxi Medical University CKD/SXMU-2024-01
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disorder and a major global health challenge, yet effective pharmacological therapies are lacking. Empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, has shown systemic metabolic and anti-inflammatory benefits, but its liver-specific molecular mechanisms remain incompletely understood. In this study, we evaluated the therapeutic effects of empagliflozin in a diet-induced mouse model of NAFLD, supported by Mendelian randomization analysis. Histological examination, serum biochemistry, and hepatic triglyceride quantification demonstrated that empagliflozin markedly attenuated hepatic steatosis and improved liver injury indices. At the molecular level, empagliflozin suppressed NF-κB-mediated inflammatory signaling and significantly downregulated fibrotic markers including α-SMA and COL1A1, while modulating TIMP-1 and MMP-9 expression. Collectively, these findings reveal that empagliflozin ameliorates NAFLD by inhibiting inflammatory and fibrotic molecular pathways, highlighting its potential as a mechanism-based therapeutic option for NAFLD.

Indexed as

COL1A1empagliflozinfibrosisinflammationMendelian randomizationNF-κBnon-alcoholic fatty liver diseaseSGLT2 inhibitorα-SMA

Identifiers

PMID41150795
PMCPMC12564516

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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 OpenQuestion graph.