Evidence map›Paper›PMID 28097824›Full record

ReviewJournal of diabetes investigation2017

Mechanisms of metabolic memory and renal hypoxia as a therapeutic target in diabetic kidney disease.

Yosuke Hirakawa, Tetsuhiro Tanaka, Masaomi Nangaku

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Novel Insights into Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  3. DNA Methylation Profiles ofBiomedicines · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Mitochondrial DNA: A New Predictor of Diabetic Kidney Disease.International journal of endocrinology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Clinico-pathological features of kidney disease in diabetic cases.Clinical and experimental nephrology · 2018
    Review
  18. International journal of molecular sciences · 2018
    Article
  19. Renal biopsy-driven molecular target identification in glomerular disease.Pflugers Archiv : European journal of physiology · 2017
    Review
  20. 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

3 authors at 2 institutions in 1 country.

Yosuke HirakawaDivision of Nephrology and Endocrinology, the University of Tokyo School of Medicine, Tokyo, Japan.
Tetsuhiro TanakaDivision of Nephrology and Endocrinology, the University of Tokyo School of Medicine, Tokyo, Japan.
Masaomi NangakuDivision of Nephrology and Endocrinology, the University of Tokyo School of Medicine, Tokyo, Japan.
University of Tokyo Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a worldwide public health problem. The definition of DKD is under discussion. Although the term DKD was originally defined as 'kidney disease specific to diabetes,' DKD frequently means chronic kidney disease with diabetes mellitus and includes not only classical diabetic nephropathy, but also kidney dysfunction as a result of nephrosclerosis and other causes. Metabolic memory plays a crucial role in the progression of various complications of diabetes, including DKD. The mechanisms of metabolic memory in DKD are supposed to include advanced glycation end-products, deoxyribonucleic acid methylation, histone modifications and non-coding ribonucleic acid including micro ribonucleic acid. Regardless of the presence of diabetes mellitus, the final common pathway in chronic kidney disease is chronic kidney hypoxia, which influences epigenetic processes, including deoxyribonucleic acid methylation, histone modification, and conformational changes in micro ribonucleic acid and chromatin. Therefore, hypoxia and oxidative stress are appropriate targets of therapies against DKD. Prolyl hydroxylase domain inhibitor enhances the defensive mechanisms against hypoxia. Bardoxolone methyl protects against oxidative stress, and can even reverse impaired renal function; a phase 2 trial with considerable attention to heart complications is currently ongoing in Japan.

Indexed as

Oxidative StressAnimalsDiabetic NephropathiesEpigenesis, GeneticHumansHypoxiaDiabetic kidney diseaseMetabolic memoryRenal hypoxia

Identifiers

PMID28097824
PMCPMC5415475
OpenAlexW2579399297

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.