Evidence map›Paper›PMID 25621126›Full record

ReviewJournal of diabetes investigation2015

Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes.

Yoshiro Maezawa, Minoru Takemoto, Koutaro Yokote

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.

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  20. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
    Review

48 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

3 authors at 2 institutions in 1 country.

Yoshiro MaezawaDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine Chiba, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital Chiba, Japan.
Minoru TakemotoDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine Chiba, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital Chiba, Japan.
Koutaro YokoteDepartment of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine Chiba, Japan ; Division of Diabetes, Metabolism and Endocrinology, Chiba University Hospital Chiba, Japan.
Chiba University · JPChiba University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is the major cause of end-stage renal failure throughout the world in both developed and developing countries. Diabetes affects all cell types of the kidney, including endothelial cells, tubulointerstitial cells, podocytes and mesangial cells. During the past decade, the importance of podocyte injury in the formation and progression of diabetic nephropathy has been established and emphasized. However, recent findings provide additional perspectives on pathogenesis of diabetic nephropathy. Glomerular endothelial damage is already present in the normoalbuminuric stage of the disease when podocyte injury starts. Genetic targeting of mice that cause endothelial injury leads to accelerated diabetic nephropathy. Tubulointerstitial damage, previously considered to be a secondary effect of glomerular protein leakage, was shown to have a primary significance in the progression of diabetic nephropathy. Emerging evidence suggests that the glomerular filtration barrier and tubulointerstitial compartment is a composite, dynamic entity where any injury of one cell type spreads to other cell types, and leads to the dysfunction of the whole apparatus. Accumulation of novel knowledge would provide a better understanding of the pathogenesis of diabetic nephropathy, and might lead to a development of a new therapeutic strategy for the disease.

Indexed as

Cell type specificConditional targetingDiabetic nephropathy

Identifiers

PMID25621126
PMCPMC4296695
OpenAlexW2005753081

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.