Evidence map›Paper›PMID 36787250›Full record

ReviewThe Journal of clinical investigation2023

Molecular pathways that drive diabetic kidney disease.

Samer Mohandes, Tomohito Doke, Hailong Hu, Dhanunjay Mukhi, Poonam Dhillon, Katalin Susztak

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 4 pooled it
58.8field-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

220 citing papers in PubMed, 4 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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160 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 2 countries.

Samer MohandesRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Tomohito DokeRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Hailong HuRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Dhanunjay MukhiRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Poonam DhillonRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Katalin SusztakRenal, Electrolyte, and Hypertension Division, Department of Medicine.
Institute of Nutrition, Metabolism and Diabetes · CA

Funding

Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
Cell Signaling in the KidneyP50DK064236 · NIDDK · YESHIVA UNIVERSITY · PI SCHUSTER, VICTOR L · 2003 to 2007
$5.7M
APOL1 associated kidney diseaseR01DK105821 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2016 to 2024
$4.6M
The role of cytosolic nucleotide sensors in inflammatory fibrosisR01DK132630 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2022 to 2025
$2.0M
NIDDK NIH HHS P50 DK064236NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK105821NIDDK NIH HHS R01 DK132630
6 · The paper itself

Abstract

Kidney disease is a major driver of mortality among patients with diabetes and diabetic kidney disease (DKD) is responsible for close to half of all chronic kidney disease cases. DKD usually develops in a genetically susceptible individual as a result of poor metabolic (glycemic) control. Molecular and genetic studies indicate the key role of podocytes and endothelial cells in driving albuminuria and early kidney disease in diabetes. Proximal tubule changes show a strong association with the glomerular filtration rate. Hyperglycemia represents a key cellular stress in the kidney by altering cellular metabolism in endothelial cells and podocytes and by imposing an excess workload requiring energy and oxygen for proximal tubule cells. Changes in metabolism induce early adaptive cellular hypertrophy and reorganization of the actin cytoskeleton. Later, mitochondrial defects contribute to increased oxidative stress and activation of inflammatory pathways, causing progressive kidney function decline and fibrosis. Blockade of the renin-angiotensin system or the sodium-glucose cotransporter is associated with cellular protection and slowing kidney function decline. Newly identified molecular pathways could provide the basis for the development of much-needed novel therapeutics.

Indexed as

Diabetes MellitusDiabetic NephropathiesPodocytesAlbuminuriaEndothelial CellsHumansKidney

Identifiers

PMID36787250
PMCPMC9927939
OpenAlexW4320709875

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.