Evidence map›Paper›PMID 31592045›Full record

ArticleDiabetology international2019

Pathophysiological roles of nutrient-sensing mechanisms in diabetes and its complications.

Shinji Kume

Abstract read
In one paragraph

Article in Diabetology international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  5. Significance of Metformin Use in Diabetic Kidney Disease.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

1 author.

Shinji KumeDepartment of Medicine, Shiga University of Medical Science, Tsukinowa-cho, Seta, Otsu, 520-2192 Shiga Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy, which is characterized by increased albuminuria, has been the most common cause of end-stage kidney disease for many years in Japan and many other countries. Although the renal prognosis of the disease has been improving in recent years because of the clinical implementation of strict glucose, blood pressure, and lipid controls, some diabetes patients continue to exhibit treatment-resistant macroalbuminuria leading to end-stage kidney disease. Furthermore, renal function decline without macroalbuminuria in diabetes is an emerging issue in Japan, which might be partly due to aging. Thus, a novel therapeutic strategy is needed to further improve renal outcome in diabetes patients. We have recently reported the involvement of dysregulation of intracellular nutrient-sensing signals and the related cellular process, autophagy, in the pathogenesis of diabetic nephropathy and abnormal insulin secretion pattern in type 2 diabetes. This review discusses potential roles of intracellular nutrient-sensing signals and autophagy as novel therapeutic targets for type 2 diabetes and diabetic nephropathy.

Indexed as

AMPKAutophagyDiabetic nephropathymTORC1Sirt1Type 2 diabetes

Identifiers

PMID31592045
PMCPMC6763549

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.