Evidence map›Paper›PMID 26719364›Full record

ReviewAmerican journal of physiology. Renal physiology2016

Transforming growth factor-β1 and diabetic nephropathy.

Albert S Chang, Catherine K Hathaway, Oliver Smithies, Masao Kakoki

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
5.3field-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

87 citing papers in PubMed, 193 citations in OpenAlex.

  1. Trial
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  4. Review
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  7. Adenosine ACells · 2025
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  14. Ethyl Acetate Fractions ofInternational journal of molecular sciences · 2024
    Article
  15. Article
  16. Article
  17. Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. [The Role of TGF-β1/SMAD in Diabetic Nephropathy: Mechanisms and Research Development].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023
    Article

27 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 1 institution in 1 country.

Albert S ChangDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Catherine K HathawayDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Oliver SmithiesDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Masao KakokiDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina mkakoki@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
NHLBI NIH HHS R01 HL049277
6 · The paper itself

Abstract

Transforming growth factor-β1 (TGF-β1) is established to be involved in the pathogenesis of diabetic nephropathy. The diabetic milieu enhances oxidative stress and induces the expression of TGF-β1. TGF-β1 promotes cell hypertrophy and extracellular matrix accumulation in the mesangium, which decreases glomerular filtration rate and leads to chronic renal failure. Recently, TGF-β1 has been demonstrated to regulate urinary albumin excretion by both increasing glomerular permeability and decreasing reabsorption in the proximal tubules. TGF-β1 also increases urinary excretion of water, electrolytes and glucose by suppressing tubular reabsorption in both normal and diabetic conditions. Although TGF-β1 exerts hypertrophic and fibrogenic effects in diabetic nephropathy, whether suppression of the function of TGF-β1 can be an option to prevent or treat the complication is still controversial. This is partly because adrenal production of mineralocorticoids could be augmented by the suppression of TGF-β1. However, differentiating the molecular mechanisms for glomerulosclerosis from those for the suppression of the effects of mineralocorticoids by TGF-β1 may assist in developing novel therapeutic strategies for diabetic nephropathy. In this review, we discuss recent findings on the role of TGF-β1 in diabetic nephropathy.

Indexed as

AnimalsDiabetic NephropathiesHumansKidneyOxidative StressSodium-Glucose Transporter 1Sodium-Glucose Transporter 2Transforming Growth Factor beta1Sodium-Glucose Transporter 1Sodium-Glucose Transporter 2Transforming Growth Factor beta1megalinnephrinpodocyteproximal tubulesodium-glucose cotransporter

Identifiers

PMID26719364
PMCPMC4835922
OpenAlexW2258832448

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.