Evidence map›Paper›PMID 29380373›Full record

ArticleJournal of cellular physiology2018

Metformin attenuates folic-acid induced renal fibrosis in mice.

Hao Yi, Chunling Huang, Ying Shi, Qinghua Cao, Yongli Zhao, Ling Zhang, Jason Chen, Carol A Pollock, Xin-Ming Chen

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 9% 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.

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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021
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  14. Article
  15. Metformin: A Novel Weapon Against Inflammation.Frontiers in pharmacology · 2021
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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 4 institutions in 2 countries.

Hao YiKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.ORCID http://orcid.org/0000-0002-9998-0461
Chunling HuangKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
Ying ShiKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
Qinghua CaoKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
Yongli ZhaoDepartment of Pediatrics, The second Hospital of Dalian Medical University, Dalian, Liaoning, P.R. China.
Ling ZhangSchool of Pharmaceutical Science &Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, P.R. China.
Jason ChenDepartment of Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia.
Carol A PollockKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
Xin-Ming ChenKolling Institute, Sydney Medical School-Northern University of Sydney, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
The University of Sydney · AUDalian Medical University · CNKunming Medical University · CNRoyal North Shore Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive tubulointerstitial fibrosis has been recognized as a common pathological process that leads to the progression of all chronic kidney disease (CKD). Innovative strategies are needed to both prevent and treat CKD. Inflammatory and fibrotic signaling pathways play central roles in the progression of CKD regardless of aetiology. Hence, targeting inflammatory and fibrotic responses holds promise to limit renal fibrosis. Metformin has been the most prescribed glucose-lowering medicine worldwide, and its potential for many other therapeutic applications is also being explored intensively. Increasing evidence indicates metformin may limit renal fibrosis. However, the exact mechanisms whereby metformin limits renal injury are not fully understood. The anti-fibrotic effects of metformin, independent of improved glycaemic control was examined in a folic acid-induced mouse model of nephropathy for 14 days. Human proximal tubular cells (HK2 cells) exposed to TGF-β1 were used in in vitro models to examine mechanistic pathways. Folic acid induced nephropathy was associated with the overexpression of inflammatory markers MCP-1, F4/80, type IV collagen, fibronectin and TGF-β1 compared to control groups, which were partially attenuated by metformin treatment. In vitro studies confirmed that metformin inhibited TGF-β1 induced inflammatory and fibrotic responses through Smad3, ERK1/2, and P38 pathways in human renal proximal tubular cells. These results suggest that metoformin attenuates folic acid-induced renal interstitial fibrogenesis through TGF-β1 signaling pathways.

Indexed as

AlbuminuriaAnimalsCell LineChemokine CCL2Collagen Type IVDisease Models, AnimalExtracellular MatrixFibronectinsFibrosisFolic AcidGene Expression RegulationHumansInflammationKidneyKidney Tubules, ProximalMaleCCL2 protein, humanChemokine CCL2Collagen Type IVFibronectinsFolic AcidMetforminSmad3 ProteinTransforming Growth Factor beta1folic acidmetforminrenal fibrosissignaling pathwaysTGF-β1

Identifiers

PMID29380373
PMCPMC13482478
OpenAlexW2790671640

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.