Evidence map›Paper›PMID 24720460›Full record

ReviewCardiovascular & hematological disorders drug targets2014

Renal endothelial dysfunction in diabetic nephropathy.

Huifang Cheng, Raymond C Harris

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular & hematological disorders drug targets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

85 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  8. Review
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  13. Review
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  15. Article
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  17. Article
  18. Article
  19. The therapeutic effect of mesenchymal stem cells in diabetic kidney disease.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  20. Review

25 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.

Huifang Cheng
Raymond C HarrisDivision of Nephrology, S3223 MCN, Vanderbilt University School of Medicine, and Nashville Veterans Affairs Hospital, Nashville, TN 37232, USA. huifang.cheng@vanderbilt.edu.
Vanderbilt University · US

Funding

TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
The Role of the EGF Receptor in Acute and Chronic Renal InjuryR01DK051265 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 1997 to 2026
$10.1M
The role of the innate immune cell cyclooxygenase/prostaglandin system in blood pressureregulationR01DK062794 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2003 to 2026
$9.4M
The Role of renal macrophages in recovery from renal injuryR01DK095785 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2013 to 2026
$6.7M
Novel Integrated Analyses of Human Diabetic NephropathyR24DK103067 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CAPRIOLI, RICHARD M, DENNY, JOSHUA C. · 2014 to 2018
$6.5M
Vanderbilt O'Brien Mouse Kidney Physiology and Disease CenterP30DK079341 · NIDDK · VANDERBILT UNIVERSITY · PI HARRIS, RAYMOND C. · 2008 to 2013
$4.4M
The Role of Cyclooxygenase-2 in Podocyte Injury in Diabetic NephropathyI01BX000320 · VA · VETERANS HEALTH ADMINISTRATION · PI RAYMOND C. HARRIS · 2009 to 2026
–
BLRD VA I01 BX000320Intramural VA VA999999NIDDK NIH HHS DK38226NIDDK NIH HHS DK51265NIDDK NIH HHS DK62794NIDDK NIH HHS DK79341NIDDK NIH HHS DK95785NIDDK NIH HHS P01 DK038226NIDDK NIH HHS P30 DK079341NIDDK NIH HHS R01 DK051265NIDDK NIH HHS R01 DK062794NIDDK NIH HHS R01 DK095785NIDDK NIH HHS R24 DK103067
6 · The paper itself

Abstract

Endothelial dysfunction has been posited to play an important role in the pathogenesis of diabetic nephropathy (DN). Due to the heterogeneity of endothelial cells (ECs), it is difficult to generalize about endothelial responses to diabetic stimuli. At present, there are limited techniques fordirectly measuring EC function in vivo, so diagnosis of endothelial disorders still largely depends on indirect assessment of mediators arising from EC injury. In the kidney microcirculation, both afferent and efferent arteries, arterioles and glomerular endothelial cells (GEnC) have all been implicated as targets of diabetic injury. Both hyperglycemia per se, as well as the metabolic consequences of glucose dysregulation, are thought to lead to endothelial cell dysfunction. In this regard, endothelial nitric oxide synthase (eNOS) plays a central role in EC dysfunction. Impaired eNOS activity can occur at numerous levels, including enzyme uncoupling, post-translational modifications, internalization and decreased expression. Reduced nitric oxide (NO) bioavailability exacerbates oxidative stress, further promoting endothelial dysfunction and injury. The injured ECs may then function as active signal transducers of metabolic, hemodynamic and inflammatory factors that modify the function and morphology of the vessel wall and interact with adjacent cells, which may activate a cascade of inflammatory and proliferative and profibrotic responses in progressive DN. Both pharmacological approaches and potential regenerative therapies hold promise for restoration of impaired endothelial cells in diabetic nephropathy.

Indexed as

AnimalsDiabetic NephropathiesEndothelial CellsHumansKidneyNitric OxideNitric Oxide Synthase Type IIIVascular Endothelial Growth Factor ANitric OxideNitric Oxide Synthase Type IIIVascular Endothelial Growth Factor A

Identifiers

PMID24720460
PMCPMC4657140
OpenAlexW1963970407

What OpenQuestion holds

Textmetadata
LicenceTDM
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.