Evidence map›Paper›PMID 17686959›Full record

ArticleAmerican journal of physiology. Renal physiology2007

17beta-Estradiol attenuates diabetic kidney disease by regulating extracellular matrix and transforming growth factor-beta protein expression and signaling.

Alexis Dixon, Christine Maric

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
3.8field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Sex-Associated Biomarker Differences in CKD Progression and Mortality.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  3. Kidney Health and Gender-Affirming Hormone Therapy for Transgender and Gender Diverse Individuals.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  4. Article
  5. Article
  6. Observational
  7. Sex differences in ventricular muscle energetics in a type 2 diabetic rat model.Cardiovascular diabetology. Endocrinology reports · 2025
    Article
  8. Article
  9. Prenatal dexamethasone programs autonomic dysregulation in female rats.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Role of sex hormones in diabetic nephropathy.Frontiers in endocrinology · 2023
    Review

7 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

2 authors at 1 institution in 1 country.

Alexis DixonDepartment of Medicine, Georgetown University Medical Center, 394 Bldg. D, 4000 Reservoir Rd. NW, Washington, DC 20057, USA.
Christine Maric
Georgetown University · US

Funding

ESTROGEN AND INFLAMMATION IN DIABETIC NEPHROPATHYR01DK075832 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI MARIC-BILKAN, CHRISTINE · 2007 to 2011
$1.4M
NIDDK NIH HHS R01 DK075832
6 · The paper itself

Abstract

We previously showed that supplementation with 17beta-estradiol (E2) from the onset of diabetes attenuates the development of diabetic renal disease. The aim of the present study was to examine whether E2 can also attenuate the disease process once it has developed. The present study was performed in nondiabetic and streptozotocin-induced diabetic Sprague-Dawley rats. E2 supplementation began after 9 wk of diabetes and continued for 8 wk. Diabetes was associated with an increase in urine albumin excretion, glomerulosclerosis, tubulointerstitial fibrosis, renal cortical collagen type I and IV, laminin, plasminogen activator inhibitor-1, tissue inhibitors of metalloproteinase-1 and -2, transforming growth factor (TGF)-beta, TGF-beta receptor type I and II, Smad2/3, phosphorylated Smad2/3, and Smad4 protein expression, and CD68-positive cell abundance. Decreases in matrix metalloproteinase (MMP)-2 protein expression and activity and decreases in Smad6 and Smad7 protein expression were also associated with diabetes. E2 supplementation completely or partially attenuated all these changes, except Smad4 and fibronectin, on which E2 supplementation had no effect. These data suggest that E2 attenuates the progression of diabetic renal disease once it has developed by regulating extracellular matrix, TGF-beta, and expression of its downstream regulatory proteins. These findings support the notion that sex hormones in general, and E2 in particular, are important regulators of renal function and may be novel targets for the treatment and prevention of diabetic renal disease.

Indexed as

AlbuminuriaAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease ProgressionEstradiolExtracellular MatrixExtracellular Matrix ProteinsFemaleFibrosisGlomerulosclerosis, Focal SegmentalKidney TubulesMatrix MetalloproteinasesNephritisPlasminogen Activator Inhibitor 1RatsEstradiolExtracellular Matrix ProteinsMatrix MetalloproteinasesPlasminogen Activator Inhibitor 1Receptors, Transforming Growth Factor betaSmad ProteinsTissue Inhibitor of MetalloproteinasesTransforming Growth Factor beta

Identifiers

PMID17686959
PMCPMC3179625
OpenAlexW2160006574

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.