Evidence map›Paper›PMID 35265754›Full record

ReviewHeliyon2022

Mitochondria-targeted drugs for diabetic kidney disease.

Akira Mima

Open access · goldAbstract readReview
In one paragraph

Review in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 82 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Akira MimaDepartment of Nephrology, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Osaka University of Pharmaceutical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is one of the most frequent causes of chronic kidney disease (CKD) in the United States. Chronic hyperglycemic conditions are thought to be the primary cause of DKD. However, it is clinically difficult to achieve glycemic control in individuals with diabetes. Recent advances in mitochondrial biology have provided a new understanding of mitochondrial dysfunction in DKD. Studies have revealed impaired mitochondrial function in a variety of diabetic complications, including DKD; moreover, abnormal mitochondrial fission may be involved in the progression of DKD. It has been reported that metformin or sodium-glucose cotransporter 2 (SGLT2) inhibitors may provide renal protection by improving mitochondrial dynamics and reducing oxidative stress. Thus, drugs that target the restoration of mitochondrial function may become novel therapeutic agents for DKD. Imeglimin is the first in a new class of oral antidiabetic drugs that can reduce reactive oxygen species production and increase mitochondrial DNA synthesis. This review outlines the potential therapeutic interventions that affect mitochondrial function and prevent DKD.

Indexed as

Diabetic kidney disease (DKD)ImegliminMetforminMitochondrial functionNFE-2 related factor 2 (Nrf2)Reactive oxygen species (ROS)Sodium-glucose cotransporter 2 (SGLT2)

Identifiers

PMID35265754
PMCPMC8899696
OpenAlexW4210777505

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.