Evidence map›Paper›PMID 30073137›Full record

ReviewAnalytical cellular pathology (Amsterdam)2018

Methylation-Demethylation Dynamics: Implications of Changes in Acute Kidney Injury.

Anubhav Chakraborty, Pragasam Viswanathan

Abstract readReview
In one paragraph

Review in Analytical cellular pathology (Amsterdam), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022
    Review
  10. 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

2 authors.

Anubhav ChakrabortyRenal Research Lab, Centre for Bio-Medical Research, School of Bio-Sciences and Technology, Vellore Institute of Technology, Vellore 632014, India.ORCID 0000-0002-3951-4469
Pragasam ViswanathanRenal Research Lab, Centre for Bio-Medical Research, School of Bio-Sciences and Technology, Vellore Institute of Technology, Vellore 632014, India.ORCID 0000-0003-3796-5589

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the years, the epigenetic landscape has grown increasingly complex. Until recently, methylation of DNA and histones was considered one of the most important epigenetic modifications. However, with the discovery of enzymes involved in the demethylation process, several exciting prospects have emerged that focus on the dynamic regulation of methylation and its crucial role in development and disease. An interplay of the methylation-demethylation machinery controls the process of gene expression. Since acute kidney injury (AKI), a major risk factor for chronic kidney disease and death, is characterised by aberrant expression of genes, understanding the dynamics of methylation and demethylation will provide new insights into the intricacies of the disease. Research on epigenetics in AKI has only made its mark in the recent years but has provided compelling evidence that implicates the involvement of methylation and demethylation changes in its pathophysiology. In this review, we explore the role of methylation and demethylation machinery in cellular epigenetic control and further discuss the contribution of methylomic changes and histone modifications to the pathophysiology of AKI.

Indexed as

Acute Kidney InjuryAnimalsDemethylationDNA MethylationEpigenesis, GeneticHumans

Identifiers

PMID30073137
PMCPMC6057397

What OpenQuestion holds

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Registered trials

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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.