Evidence map›Paper›PMID 31116068›Full record

ReviewThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2019

Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.

Jianyong Zhong, Jacob B Whitman, Hai-Chun Yang, Agnes B Fogo

Open access · bronzeAbstract readReview
In one paragraph

Review in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The Pathology Lesion Patterns of Podocytopathies: How and why?Frontiers in cell and developmental biology · 2022
    Review
  11. 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

4 authors at 1 institution in 1 country.

Jianyong ZhongDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Jacob B WhitmanDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Hai-Chun YangDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Agnes B FogoDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Vanderbilt University Medical Center · US

Funding

Vanderbilt O'Brien Kidney Center - Core D - Clinical and Translational CoreP30DK114809 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CAESTECKER, MARK P. · 2017 to 2021
$5.9M
RESOLUTION OF GLOMERULOSCLEROSISR01DK056942 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI FOGO, AGNES B. · 2001 to 2021
$4.9M
NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK056942
6 · The paper itself

Abstract

Focal segmental glomerulosclerosis (FSGS) presents with scar in parts of some glomeruli and often progresses to global and diffuse glomerulosclerosis. Podocyte injury is the initial target in primary FSGS, induced by a circulating factor. Several gene variants, for example, APOL1, are associated with increased susceptibility to FSGS. Primary FSGS may be due to genetic mutation in key podocyte genes. Increased work stress after loss of nephrons, epigenetic mechanisms, and various profibrotic pathways can contribute to progressive sclerosis, regardless of the initial injury. The progression of FSGS lesions also involves crosstalk between podocytes and other kidney cells, such as parietal epithelial cells, glomerular endothelial cells, and even tubular epithelial cells. New insights related to these mechanisms could potentially lead to new therapeutic strategies to prevent progression of FSGS.

Indexed as

AnimalsApolipoprotein L1CicatrixDisease ProgressionEndothelial CellsEpigenesis, GeneticEpithelial CellsGlomerulosclerosis, Focal SegmentalHumansKidney GlomerulusKidney TubulesPodocytesAPOL1 protein, humanApolipoprotein L1chronic kidney diseaseendothelial cellextracellular matrixfibrosisFSGSparietal epithelial cellpodocytetransforming growth factor betatubular epithelial cell

Identifiers

PMID31116068
PMCPMC6713971
OpenAlexW2946170303

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.