Evidence map›Paper›PMID 37511155›Full record

ArticleInternational journal of molecular sciences2023

Smad3 Mediates Diabetic Dyslipidemia and Fatty Liver in db/db Mice by Targeting PPARδ.

Huijun He, Yu Zhong, Honglian Wang, Patrick Ming-Kuen Tang, Vivian Weiwen Xue, Xiaocui Chen, Jiaoyi Chen, Xiaoru Huang, Cheng Wang, Huiyao Lan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Nur77 Regulates the Phosphorylation of Smad3, Thereby Influencing Skeletal Muscle Fibrosis Caused by Obesity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  7. 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

10 authors at 2 institutions in 2 countries.

Huijun HeDivision of Nephrology, Department of Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China.ORCID 0000-0003-1910-3897
Yu ZhongDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0001-6902-2732
Honglian WangDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.
Patrick Ming-Kuen TangState Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0002-3194-3736
Vivian Weiwen XueState Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0002-0737-3593
Xiaocui ChenDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.
Jiaoyi ChenDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0001-5601-9411
Xiaoru HuangDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.
Cheng WangDivision of Nephrology, Department of Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China.ORCID 0000-0002-1590-7954
Huiyao LanDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China.ORCID 0000-0003-4283-9755
Chinese University of Hong Kong · HKSun Yat-sen University · CN

Funding

Research Grants Council of Hong Kong GRF 14117418, 14104019, 17109019, 14101121, R4012-18the Guangdong-Hong Kong-Macao-Joint Labs Program from Guangdong Science and Technology Department 2019B121205005the Health and Medical Research Fund of Hong Kong HMRF 14152321, 06173986, 07180516the Lui Che Woo Institute of Innovative Medicine CARE program
6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)-

Indexed as

Diabetes Mellitus, Type 2Non-alcoholic Fatty Liver DiseasePPAR deltaSmad3 ProteinAnimalsLiverMiceMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutPPAR deltaSmad3 Proteindiabetesdyslipidemiafatty liverSmad3Smad3 inhibitortreatment

Identifiers

PMID37511155
PMCPMC10380492
OpenAlexW4384341227

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.