Evidence map›Paper›PMID 24780459›Full record

ReviewAdvances in chronic kidney disease2014

Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.

Frank C Brosius, Richard J Coward

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.7field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024
    Article
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  11. Review
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  17. Review
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  20. Morroniside Inhibits HFrontiers in pharmacology · 2020
    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

2 authors at 2 institutions in 2 countries.

Frank C BrosiusDepartments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI; and Children's Renal Unit, University of Bristol, Bristol, United Kingdom. Electronic address: fbrosius@umich.edu.
Richard J CowardDepartments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI; and Children's Renal Unit, University of Bristol, Bristol, United Kingdom.
University of Bristol · GBUniversity of Michigan–Ann Arbor · US

Funding

Integrated Systems Biology Approach to Diabetic Microvascular ComplicationsR24DK082841 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, BROSIUS, FRANK C · 2008 to 2020
$13.1M
University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
Tissue-Specific Metabolic Reprogramming in Diabetic ComplicationsDP3DK094292 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C, BURANT, CHARLES F · 2011 to 2011
$5.5M
Medical Research Council MR/K010492/1NIDDK NIH HHS DP3 DK094292NIDDK NIH HHS DP3DK094292NIDDK NIH HHS P30 DK081943NIDDK NIH HHS P30DK081943NIDDK NIH HHS R24 DK082841NIDDK NIH HHS R24DK082841
6 · The paper itself

Abstract

Alterations and injury to glomerular podocytes play a key role in the initiation and progression of diabetic kidney disease (DKD). Multiple factors in diabetes cause abnormalities in podocyte signaling that lead to podocyte foot process effacement, hypertrophy, detachment, loss, and death. Alterations in insulin action and mammalian target of rapamycin activation have been well documented to lead to pathology. Reduced insulin action directly leads to albuminuria, increased glomerular matrix accumulation, thickening of the glomerular basement membrane, podocyte apoptosis, and glomerulosclerosis. In addition, podocytes generate factors that alter signaling in other glomerular cells. Prominent among these is vascular endothelial growth factor-A, which maintains glomerular endothelium viability but causes endothelial cell pathology when generated at too high a level. Finally, circulating vascular factors (eg, activated protein C) have a profound effect on podocyte stability and survival. This cytoprotective factor is critical for podocyte health, and its deficiency promotes podocyte injury and apoptosis. Thus, the podocyte sits in the center of a network of paracrine and hormonal signaling systems that in health keep the podocyte adaptable and viable, but in diabetes they can lead to pathologic changes, detachment, and death.

Indexed as

Blood GlucoseDiabetic NephropathiesHumansInsulinPodocytesSignal TransductionTOR Serine-Threonine KinasesVascular Endothelial Growth Factor ABlood GlucoseInsulinMTOR protein, humanTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVEGFA protein, humanDiabetesGlomerulusGlucoseInsulinMammalian target of rapamycin

Identifiers

PMID24780459
PMCPMC4075065
OpenAlexW2066471150

What Socratic 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 Socratic graph.