Evidence map›Paper›PMID 22417893›Full record

ReviewExperimental cell research2012

The role of cell-extracellular matrix interactions in glomerular injury.

Corina M Borza, Ambra Pozzi

Open access · greenAbstract readReview
In one paragraph

Review in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Graphene-Based Materials for Efficient Neurogenesis.Advances in experimental medicine and biology · 2022
    Article
  8. Article
  9. The Role of the EGF Receptor in Sex Differences in Kidney Injury.Journal of the American Society of Nephrology : JASN · 2019
    Article
  10. Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Integrins in kidney disease.Journal of the American Society of Nephrology : JASN · 2013
    Review
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.

Corina M BorzaDepartment of Medicine, Division of Nephrology, Vanderbilt University, Nashville, TN 37232, USA. corina.borza@vanderbilt.edu
Ambra Pozzi
Vanderbilt University · US

Funding

TYPE IV COLLAGEN, LAMININS, AND INTEGRINS IN NORMAL AND DISEASED GLOMERULIP01DK065123 · NIDDK · VANDERBILT UNIVERSITY · PI HUDSON, BILLY GERALD · 2003 to 2012
$12.9M
Vanderbilt O'Brien Mouse Kidney Physiology and Disease CenterP30DK079341 · NIDDK · VANDERBILT UNIVERSITY · PI HARRIS, RAYMOND C. · 2008 to 2013
$4.4M
NIDDK NIH HHS 2P01DK065123NIDDK NIH HHS P01 DK065123NIDDK NIH HHS P30 DK079341NIDDK NIH HHS P30DK79341-01
6 · The paper itself

Abstract

Glomerulosclerosis is characterized by excessive deposition of extracellular matrix within the glomeruli of the kidney, glomerular cell death, and subsequent loss of functional glomeruli. While in physiological situations the levels of extracellular matrix components are kept constant by a tight balance between formation and degradation, in the case of injury that results in fibrosis there is increased matrix deposition relative to its breakdown. Multiple factors control matrix synthesis and degradation, thus contributing to the development of glomerulosclerosis. This review focuses primarily on the role of cell-matrix interactions, which play a critical role in governing glomerular cell cues in both healthy and diseased kidneys. Cell-extracellular matrix interactions are made possible by various cellular receptors including integrins, discoidin domain receptors, and dystroglycan. Upon binding to a selective extracellular matrix protein, these receptors activate intracellular signaling pathways that can either downregulate or upregulate matrix synthesis and deposition. This, together with the observation that changes in the expression levels of matrix receptors have been documented in glomerular disease, clearly emphasizes the contribution of cell-matrix interactions in glomerular injury. Understanding the molecular mechanisms whereby extracellular matrix receptors regulate matrix homeostasis in the course of glomerular injury is therefore critical for devising more effective therapies to treat and ideally prevent glomerulosclerosis.

Indexed as

AnimalsExtracellular MatrixGlomerulonephritisHumansIntegrinsKidneyKidney DiseasesKidney GlomerulusIntegrins

Identifiers

PMID22417893
PMCPMC3770307
OpenAlexW2016580242

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.