ArticleTransactions of the American Clinical and Climatological Association2023
SUPPRESION OF MITOCHONDRIAL RESPIRATION IS A FEATURE OF CELLULAR GLUCOSE TOXICITY.
Article in Transactions of the American Clinical and Climatological Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed, 0 citations in OpenAlex.
- Role of metabolic conditions in cardiorenal diseases: initiating pathways and therapeutic targeting.Frontiers in nutrition · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Glucose toxicity is central to the myriad complications of diabetes and is now believed to encompass neurodegenerative diseases and cancer as well as microvascular and macrovascular disease. Due to the widespread benefits of SGLT2 inhibitors, which affect glucose uptake in the kidney proximal tubular cell, a focus on cell metabolism in response to glucose has important implications for overall health. We previously found that a -Warburg-type effect underlies diabetic kidney disease and involves metabolic reprogramming. This is now supported by quantitative measurements of superoxide measurement in the diabetic kidney and systems biology analysis of urine metabolites in patients. Further exploration of mechanisms underlying mediators of mitochondrial suppression will be critical in understanding the chronology of glucose-induced toxicity and developing new therapeutics to arrest the systemic glucose toxicity of diabetes.
Indexed as
Identifiers
37701600PMC10493723W4386703818What OpenQuestion holds
Registered trials
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.