Evidence map›Paper›PMID 36614011›Full record

ReviewInternational journal of molecular sciences2022

What's New in the Molecular Mechanisms of Diabetic Kidney Disease: Recent Advances.

Kimio Watanabe, Emiko Sato, Eikan Mishima, Mariko Miyazaki, Tetsuhiro Tanaka

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
–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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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

5 authors.

Kimio WatanabeDialysis Center, Tohoku University Hospital, Sendai 980-8574, Japan.ORCID 0000-0002-8773-0967
Emiko SatoDivision of Clinical Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.
Eikan MishimaDivision of Nephrology, Rheumatology and Endocrinology, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.ORCID 0000-0002-3706-2745
Mariko MiyazakiDialysis Center, Tohoku University Hospital, Sendai 980-8574, Japan.
Tetsuhiro TanakaDivision of Nephrology, Rheumatology and Endocrinology, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease, including end-stage kidney disease, and increases the risk of cardiovascular mortality. Although the treatment options for DKD, including angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, sodium-glucose cotransporter 2 inhibitors, and mineralocorticoid receptor antagonists, have advanced, their efficacy is still limited. Thus, a deeper understanding of the molecular mechanisms of DKD onset and progression is necessary for the development of new and innovative treatments for DKD. The complex pathogenesis of DKD includes various different pathways, and the mechanisms of DKD can be broadly classified into inflammatory, fibrotic, metabolic, and hemodynamic factors. Here, we summarize the recent findings in basic research, focusing on each factor and recent advances in the treatment of DKD. Collective evidence from basic and clinical research studies is helpful for understanding the definitive mechanisms of DKD and their regulatory systems. Further comprehensive exploration is warranted to advance our knowledge of the pathogenesis of DKD and establish novel treatments and preventive strategies.

Indexed as

Diabetes MellitusDiabetic NephropathiesKidney Failure, ChronicRenal Insufficiency, ChronicAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsHumansAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor Antagonistsdiabetic kidney diseasefibrosishemodynamicsinflammationmetabolismSGLT2 inhibitor

Identifiers

PMID36614011
PMCPMC9820354

What Socratic holds

Textmetadata
LicenceCC BY
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.