Evidence map›Paper›PMID 32193834›Full record

ReviewJournal of nephrology2020

Kidney allograft fibrosis: what we learned from latest translational research studies.

Simona Granata, Claudia Benedetti, Giovanni Gambaro, Gianluigi Zaza

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  11. Epigenetic modifications and the development of kidney graft fibrosis.Current opinion in organ transplantation · 2021
    Review
  12. Article
  13. Recent Advances on Biomarkers of Early and Late Kidney Graft Dysfunction.International journal of molecular sciences · 2020
    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

4 authors at 1 institution in 1 country.

Simona Granata *Renal Unit, Department of Medicine, University Hospital of Verona, Piazzale A. Stefani 1, 37126, Verona, VR, Italy.
Claudia Benedetti *Renal Unit, Department of Medicine, University Hospital of Verona, Piazzale A. Stefani 1, 37126, Verona, VR, Italy.
Giovanni GambaroRenal Unit, Department of Medicine, University Hospital of Verona, Piazzale A. Stefani 1, 37126, Verona, VR, Italy.
Gianluigi ZazaRenal Unit, Department of Medicine, University Hospital of Verona, Piazzale A. Stefani 1, 37126, Verona, VR, Italy. gianluigi.zaza@univr.it.ORCID http://orcid.org/0000-0002-6004-6196
University of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To add new molecular and pathogenetic insights into the biological machinery associated to kidney allograft fibrosis is a major research target in nephrology and organ transplant translational medicine. Interstitial fibrosis associated to tubular atrophy (IF/TA) is, in fact, an inevitable and progressive process that occurs in almost every type of chronic allograft injury (particularly in grafts from expanded criteria donors) characterized by profound remodeling and excessive production/deposition of fibrillar extracellular matrix (ECM) with a great clinical impact. IF/TA is detectable in more than 50% of kidney allografts at 2 years. However, although well studied, the complete cellular/biological network associated with IF/TA is only partially evaluated. In the last few years, then, thanks to the introduction of new biomolecular technologies, inflammation in scarred/fibrotic parenchyma areas (recently acknowledged by the BANFF classification) has been recognized as a pivotal element able to accelerate the onset and development of the allograft chronic damage. Therefore, in this review, we focused on some new pathogenetic elements involved in graft fibrosis (including epithelial/endothelial to mesenchymal transition, oxidative stress, activation of Wnt and Hedgehog signaling pathways, fatty acids oxidation and cellular senescence) that, in our opinion, could become in future good candidates as potential biomarkers and therapeutic targets.

Indexed as

Kidney TransplantationTranslational Research, BiomedicalAllograftsAtrophyFibrosisGraft RejectionHedgehog ProteinsHumansKidneyKidney TubulesHedgehog ProteinsCellular senescenceFatty acids oxidationhedgehog signaling pathwaysInterstitial fibrosis and tubular atrophyKidney fibrosisWnt pathway

Identifiers

PMID32193834
OpenAlexW3011843696

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.