Evidence map›Paper›PMID 35541902›Full record

ReviewInternational journal of biological sciences2022

Smad3 Signatures in Renal Inflammation and Fibrosis.

Wenjing Wu, Xiaoqin Wang, Xueqing Yu, Hui-Yao Lan

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 2 pooled it
22.5field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 2 syntheses or guidelines pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  5. Article
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  8. Ginsenoside RgJournal of natural medicines · 2026
    Article
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  11. Review
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  19. Abietane-Type Diterpenoids from the Resin ofMolecules (Basel, Switzerland) · 2026
    Article
  20. Article

49 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

Wenjing WuGuangdong-Hong Kong Joint Laboratory for Immunological and Genetic Kidney Disease, Department of Pathology, and Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangdong Provincial People's Hospital, Guangzhou, China.
Xiaoqin WangHubei University of Chinese Medicine, Wuhan, China.
Xueqing YuGuangdong-Hong Kong Joint Laboratory for Immunological and Genetic Kidney Disease, Department of Pathology, and Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangdong Provincial People's Hospital, Guangzhou, China.
Hui-Yao LanDepartments of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Chinese University of Hong Kong · CNGuangdong Provincial People's Hospital · CNHubei University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal inflammation and fibrosis are key pathological features of acute kidney injury (AKI) and chronic kidney disease (CKD). Smad3 is a critical mediator of TGF-β signaling and plays a pathogenic role in both renal inflammation and fibrosis. Smad3 can be activated not only by TGF-β1 but also by many stress molecules including angiotensin II (Ang II), advanced end products (AGEs), and C-reactive protein (CRP) under disease conditions. In addition, Smad3 can interact with other signaling pathways, such as the ERK/p38 MAPK and NF-κB pathways, to mediate renal inflammation and fibrosis. Mechanistically, Smad3 transcriptionally regulates many downstream target genes including microRNAs and long non-coding RNAs to cause cell death, inflammation, and fibrosis. Thus, targeting Smad3 or its downstream genes specifically related to renal inflammation and fibrosis should provide a novel therapeutic strategy to combat kidney diseases.

Indexed as

Renal Insufficiency, ChronicSmad3 ProteinFemaleFibrosisHumansInflammationKidneyMaleNF-kappa BSignal TransductionTransforming Growth Factor beta1NF-kappa BSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor beta1lncRNAsmiRNAsrenal inflammation and fibrosisSmad3

Identifiers

PMID35541902
PMCPMC9066101
OpenAlexW4226517342

What Socratic 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 Socratic graph.