Evidence map›Paper›PMID 34356375›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Metabolic Changes and Oxidative Stress in Diabetic Kidney Disease.

Midori Sakashita, Tetsuhiro Tanaka, Reiko Inagi

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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  18. Unlocking the mechanistic potential ofJournal of traditional and complementary medicine · 2024
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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.

Midori SakashitaDivision of Nephrology and Endocrinology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Tetsuhiro TanakaDivision of Nephrology and Endocrinology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Reiko InagiDivision of CKD Pathophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0001-7032-7736
The University of Tokyo · JP

Funding

Japan Society for the Promotion of Science 18H02727Japan Society for the Promotion of Science 20K08626
6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin-angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD. The pathophysiology of DKD is largely attributed to the disruption of various cellular stress responses due to metabolic changes, especially an increase in oxidative stress. Therefore, many antioxidants have been studied as therapeutic agents. Recently, it has been found that NRF2, a master regulator of oxidative stress, plays a major role in the pathogenesis of DKD and bardoxolone methyl, an activator of NRF2, has attracted attention as a drug that increases the estimated glomerular filtration rate in patients with DKD. This review outlines the altered stress responses of cellular organelles in DKD, their involvement in the pathogenesis of DKD, and discusses strategies for developing therapeutic agents, especially bardoxolone methyl.

Indexed as

bardoxolone methyldiabetic kidney diseaseNrf2organelle crosstalkoxidative stress

Identifiers

PMID34356375
PMCPMC8301131
OpenAlexW3185411180

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.