Evidence map›Paper›PMID 29396446›Full record

ArticleCell death & disease2018

SMAD4 feedback regulates the canonical TGF-β signaling pathway to control granulosa cell apoptosis.

Xing Du, Zengxiang Pan, Qiqi Li, Honglin Liu, Qifa Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  4. ELK1 regulates BMPR1B transcriptional activity in ovine granulosa cells.Frontiers in cell and developmental biology · 2025
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  9. Role of TGF-β1/SMADs signalling pathway in resveratrol-induced reduction of extracellular matrix deposition by dexamethasone-treated human trabecular meshwork cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
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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

5 authors at 1 institution in 1 country.

Xing DuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
Zengxiang PanCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
Qiqi LiCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
Honglin LiuCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.
Qifa LiCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China. liqifa@njau.edu.cn.
Nanjing Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Canonical TGF-β signals are transduced from the cell surface to the cytoplasm, and then translocated into the nucleus, a process that involves ligands (TGF-β1), receptors (TGFBR2/1), receptor-activated SMADs (SMAD2/3), and the common SMAD (SMAD4). Here we provide evidence that SMAD4, a core component of the canonical TGF-β signaling pathway, regulates the canonical TGF-β signaling pathway in porcine granulosa cells (GCs) through a feedback mechanism. Genome-wide analysis and qRT-PCR revealed that SMAD4 affected miRNA biogenesis in GCs. Interestingly, TGFBR2, the type II receptor of the canonical TGF-β signaling pathway, was downregulated in SMAD4-silenced GCs and found to be a common target of SMAD4-inhibited miRNAs. miR-425, the most significantly elevated miRNA in SMAD4-silenced GCs, mediated the SMAD4 feedback regulation of the TGF-β signaling pathway. This was accomplished through a direct interaction between the transcription factor SMAD4 and the miR-425 promoter, and a direct interaction between miR-425 and the TGFBR2 3'-UTR. Furthermore, miR-425 enhanced GC apoptosis by targeting TGFBR2 and the canonical TGF-β signaling pathway, which was rescued by SMAD4 and TGF-β1. Overall, our findings demonstrate that a positive feedback mechanism exists within the canonical TGF-β signaling pathway. This study also provides new insights into mechanism underlying the canonical TGF-β signaling pathway, which regulates GC function and follicular development.

Indexed as

ApoptosisFeedback, PhysiologicalSignal TransductionAnimalsBase SequenceEpigenesis, GeneticFemaleGranulosa CellsMicroRNAsPromoter Regions, GeneticProtein BindingReceptor, Transforming Growth Factor-beta Type IISmad4 ProteinSwineTransforming Growth Factor betaMicroRNAsReceptor, Transforming Growth Factor-beta Type IISmad4 ProteinTransforming Growth Factor beta

Identifiers

PMID29396446
PMCPMC5833407
OpenAlexW2791445933

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.