Evidence map›Paper›PMID 34189465›Full record

ReviewKidney3602020

Shaping Up Mitochondria in Diabetic Nephropathy.

Koki Mise, Daniel L Galvan, Farhad R Danesh

Open access · diamondAbstract readReview
In one paragraph

Review in Kidney360, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Amino acid metabolism in diabetic kidney disease.Clinical and experimental nephrology · 2026
    Review
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  15. Organelle Stress and Metabolic Derangement in Kidney Disease.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Review
  18. Article
  19. 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 1 institution in 1 country.

Koki MiseSection of Nephrology, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-0296-7429
Daniel L GalvanSection of Nephrology, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Farhad R DaneshSection of Nephrology, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-6849-5239
The University of Texas MD Anderson Cancer Center · US

Funding

MicroRNA In Diabetic NephropathyR01DK091310 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANESH, FARHAD R · 2011 to 2024
$5.3M
Role of Rho Kinases in Diabetic NephropathyR01DK078900 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DANESH, FARHAD R · 2009 to 2024
$5.2M
NIDDK NIH HHS R01 DK078900NIDDK NIH HHS R01 DK091310
6 · The paper itself

Abstract

Mitochondrial medicine has experienced significant progress in recent years and is expected to grow significantly in the near future, yielding many opportunities to translate novel bench discoveries into clinical medicine. Multiple lines of evidence have linked mitochondrial dysfunction to a variety of metabolic diseases, including diabetic nephropathy (DN). Mitochondrial dysfunction presumably precedes the emergence of key histologic and biochemical features of DN, which provides the rationale to explore mitochondrial fitness as a novel therapeutic target in patients with DN. Ultimately, the success of mitochondrial medicine is dependent on a better understanding of the underlying biology of mitochondrial fitness and function. To this end, recent advances in mitochondrial biology have led to new understandings of the potential effect of mitochondrial dysfunction in a myriad of human pathologies. We have proposed that molecular mechanisms that modulate mitochondrial dynamics contribute to the alterations of mitochondrial fitness and progression of DN. In this comprehensive review, we highlight the possible effects of mitochondrial dysfunction in DN, with the hope that targeting specific mitochondrial signaling pathways may lead to the development of new drugs that mitigate DN progression. We will outline potential tools to improve mitochondrial fitness in DN as a novel therapeutic strategy. These emerging views suggest that the modulation of mitochondrial fitness could serve as a key target in ameliorating progression of kidney disease in patients with diabetes.

Indexed as

Diabetes MellitusDiabetic NephropathiesHumansMitochondriaMitochondrial DynamicsSignal Transduction

Identifiers

PMID34189465
PMCPMC8238457
OpenAlexW3046152030

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.