Evidence map›Paper›PMID 35625768›Full record

ArticleBiomedicines2022

Empagliflozin Reduces the Progression of Hepatic Fibrosis in a Mouse Model and Inhibits the Activation of Hepatic Stellate Cells via the Hippo Signalling Pathway.

Yu-Jung Heo, Nami Lee, Sung-E Choi, Ja-Young Jeon, Seung-Jin Han, Dae-Jung Kim, Yup Kang, Kwan-Woo Lee, Hae-Jin Kim

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05605158 (Comparative Clinical Study to Evaluate the Possible Beneficial Effect of Empagliflozin Versus Pioglitazone on Non-diabetic Patients With Non-Alcoholic Steatohepatitis), which is not on this map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 18% of its field
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.

NCT05605158 phase3unknown statusnot on this map

Comparative Clinical Study to Evaluate the Possible Beneficial Effect of Empagliflozin Versus Pioglitazone on Non-diabetic Patients With Non-Alcoholic Steatohepatitis

TypeinterventionalSponsorTanta UniversityRan2022 to 2024Enrolled56ConditionsNon Alcoholic SteatohepatitisArmsPioglitazone 30mg, Empagliflozin 10 MG
3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  6. Review
  7. Article
  8. Article
  9. Cysteine-rich 61 inhibition attenuates hepatic insulin resistance and improves lipid metabolism in high-fat diet fed mice and HepG2 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  10. Effect of Semaglutide and Empagliflozin on Pulmonary Structure and Proteomics in Obese Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  11. Portal Hypertension in Nonalcoholic Fatty Liver Disease: Challenges and Paradigms.Journal of clinical and translational hepatology · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
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

9 authors at 1 institution in 1 country.

Yu-Jung HeoDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.
Nami LeeDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.ORCID 0000-0003-0343-5619
Sung-E ChoiDepartment of Physiology, Ajou University School of Medicine, Suwon 16499, Korea.
Ja-Young JeonDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.
Seung-Jin HanDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.ORCID 0000-0003-4783-6799
Dae-Jung KimDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.ORCID 0000-0003-1025-2044
Yup KangDepartment of Physiology, Ajou University School of Medicine, Suwon 16499, Korea.
Kwan-Woo LeeDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.
Hae-Jin KimDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon 16499, Korea.ORCID 0000-0002-8958-7164
Ajou University · KR

Funding

National Research Foundation of Korea NRF-2020R1F1A1074019, NRF2021M3H1A104892211
6 · The paper itself

Abstract

Hepatic fibrosis is the excessive production and deposition of the extracellular matrix, resulting in the activation of the fibrogenic phenotype of hepatic stellate cells (HSCs). The Hippo/Yes-associated protein (YAP) signalling pathway is a highly conserved kinase cascade that is critical in regulating cell proliferation, differentiation, and survival, and controls stellate cell activation. Empagliflozin, a sodium-glucose cotransporter type-2 inhibitor, is an antidiabetic drug that may prevent fibrotic progression by reducing hepatic steatosis and inflammation. However, little is known about its mechanism of action in liver fibrosis. In this study, we used male C57 BL/6 J mice fed a choline-deficient, l-amino acid-defined, high-fat diet (CDAHFD) as a model for hepatic fibrosis. For 5 weeks, the mice received either a vehicle or empagliflozin based on their assigned group. Empagliflozin attenuated CDAHFD-induced liver fibrosis. Thereafter, we identified the Hippo pathway, along with its effector, YAP, as a key pathway in the mouse liver. Hippo signalling is inactivated in the fibrotic liver, but empagliflozin treatment activated Hippo signalling and decreased YAP activity. In addition, empagliflozin downregulated the expression of pro-fibrogenic genes and activated Hippo signalling in HSCs. We identified a mechanism by which empagliflozin ameliorates liver fibrosis.

Indexed as

empagliflozinhepatic fibrosishepatic stellate cellsHippo signalling pathway

Identifiers

PMID35625768
PMCPMC9138578
OpenAlexW4225113118

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.