Evidence map›Paper›PMID 30258890›Full record

ReviewGenes & diseases2016

Role of autophagy and histone deacetylases in diabetic nephropathy: Current status and future perspectives.

Sabbir Khan, Zahid Rafiq Bhat, Gopabandhu Jena

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 2016. 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
1.7field-weighted citation impact, top 16% 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, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Caffeic Acid Modulates miR-636 Expression in Diabetic Nephropathy Rats.Indian journal of clinical biochemistry : IJCB · 2019
    Article
  8. Article
  9. 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

3 authors at 1 institution in 1 country.

Sabbir KhanFacility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Punjab, 160062, India.
Zahid Rafiq BhatFacility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Punjab, 160062, India.
Gopabandhu JenaFacility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Punjab, 160062, India.
National Institute of Pharmaceutical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of diabetes and its complications is increasing at an alarming rate in both developed and deve1oping nations. The emerging evidences highlighted that both genetic and epigenetic mechanisms including histone modifications play a significant role in the pathogenesis of diabetic nephropathy (DN). Histone deacetylases (HDACs) and acetylation are involved in the regulation of autophagy as well as pathogenesis of DN. Both HDACs and histone acetyltransferases (HATs) play a key role in chromatin remodeling and affect the transcription of various genes involved in the cellular homeostasis, apoptosis, immunity and angiogenesis. Further, HDAC inhibitors are exert the renoprotective effects in DN and other diabetic complications. Thus, the cellular acetylation plays a crucial role in the regulation of autophagy and can be explored as a new therapeutic target for the treatment of DN. This review aimed to delineate the role of HDACs and associated molecular signaling/pathways in the regulation of autophagy with an emphasis on promising targets for the treatment of DN.

Indexed as

AcetylationAutophagyDiabetic nephropathy and SIRTsHDAC inhibitorsHDACs

Identifiers

PMID30258890
PMCPMC6150107
OpenAlexW2341406790

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.