Evidence map›Paper›PMID 28664408›Full record

ReviewPflugers Archiv : European journal of physiology2017

Focal segmental glomerulosclerosis; why does it occur segmentally?

Michio Nagata, Namiko Kobayashi, Satoshi Hara

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022
    Review
  7. Article
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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 3 institutions in 1 country.

Michio NagataKidney and Vascular Pathology, Faculty of Medicine, University of Tsukuba, Ten-nodai 1-1-1, Tsukuba-City, Ibaraki, 305-8577, Japan. nagatam@md.tsukuba.ac.jp.ORCID http://orcid.org/0000-0002-7360-5524
Namiko KobayashiNephrology, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-850, Japan.
Satoshi HaraRheumatology, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, 920-8671, Japan.
Kanazawa University · JPTokyo Medical and Dental University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Podocyte loss is the fundamental basis of glomerulosclerosis. Focal segmental glomerulosclerosis (FSGS) is a progressive glomerular disease, and its glomerular features are a prototype of podocyte loss-driven glomerulosclerosis. The glomerular pathology of FSGS is characterized by a focal and segmental location of the sclerotic lesions in human FSGS; segmental sclerosis often shows simultaneous intra- and extra-capillary changes, including parietal cell migration, capillary collapse, hyaline deposition, and intra-capillary thrombi and occasional hypercellularity. This suggests that local cellular events, initiated by podocyte loss, are the basis of the segmental lesions in FSGS. Using podocyte-specific injury by toxin administration, a series of recent works has identified the cellular basis of the glomerular response to podocyte loss. This review discusses the molecular pathway of the local response to podocyte loss and its progression to sclerosis. Recent results suggest that segmental sclerosis is a physiological tissue response aimed at halting protein leakage from a disrupted filtration barrier.

Indexed as

AnimalsGlomerulosclerosis, Focal SegmentalHumansPodocytesSclerosisFoam cellsFocal segmental glomerulosclerosis (FSGS)MicroangiopathyParietal cellsPodocyte loss

Identifiers

PMID28664408
OpenAlexW2729682633

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.