Evidence map›Paper›PMID 30152848›Full record

ArticleMolecular medicine reports2018

Pirfenidone suppresses TGF‑β1‑induced human intestinal fibroblasts activities by regulating proliferation and apoptosis via the inhibition of the Smad and PI3K/AKT signaling pathway.

Yanwu Sun, Yiyi Zhang, Pan Chi

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 49 citations in OpenAlex.

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  8. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
    Review
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  10. [Aloe-emodin inhibits scar tissue fibrosis through thrombospondin-1-PI3k-Akt pathway].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025
    Article
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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

3 authors at 1 institution in 1 country.

Yanwu SunDepartment of Colorectal Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
Yiyi ZhangDepartment of Colorectal Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
Pan ChiDepartment of Colorectal Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal fibroblasts, the main effector cells of intestinal fibrosis, are considered to be a good target for anti‑fibrotic therapy. The aim of the present study was to examine the effects of pirfenidone (PFD) on human intestinal fibroblasts (HIFs) stimulated by transforming growth factor (TGF)‑β1 and to explore the potential mechanism. Prior to stimulation with TGF‑β1 (10 ng/ml), HIFs were treated with or without PFD (1 mg/ml). Cell proliferation was determined by Cell Counting Kit (CCK)‑8 and colony formation assays, and cell apoptosis was assessed using flow cytometry and a TUNEL assay. Reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to evaluate the mRNA and protein expressions of α‑smooth muscle actin (α‑SMA), collagen I and fibronectin. The protein expression of TGF‑β1/mothers against decapentaplegic homolog (Smad) and phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathways was evaluated by western blotting. CCK‑8 and colony formation assays demonstrated that PFD significantly inhibited cell proliferation in HIFs stimulated with TGF‑β1. Flow cytometry and TUNEL assays revealed that PFD treatment significantly enhanced apoptosis in TGF‑β1‑stimulated HIFs. In addition, PFD markedly reduced TGF‑β1‑induced HIF activities, such as myofibroblast differentiation (α‑SMA), and collagen production (collagen I and fibronectin). These effects of PFD were mediated by the inhibition of the TGF‑β1/Smad and PI3K/AKT signaling pathways. Therefore, the present study demonstrated that PFD reduced TGF‑β1‑induced fibrogenic activities of HIFs, suggesting that PFD may be a potential therapeutic agent for intestinal fibrosis.

Indexed as

ApoptosisCell DifferentiationCell ProliferationCollagenFibroblastsHumansIntestinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyridonesSignal TransductionSmad ProteinsTransforming Growth Factor beta1CollagenPhosphatidylinositol 3-KinasespirfenidoneProto-Oncogene Proteins c-aktPyridonesSmad ProteinsTransforming Growth Factor beta1

Identifiers

PMID30152848
PMCPMC6131636
OpenAlexW2888293125

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.