Aldose Reductase: a cause and a potential target for the treatment of diabetic complications.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and drug classes without original empirical data or systematic review methodology.
PubMed 34279787 · doi:10.1007/s12272-021-01343-5
What was done
This narrative review summarizes the mechanistic role of aldose reductase and polyol pathway activation in hyperglycaemia-induced pathology, along with candidate classes of aldose reductase inhibitors (such as carboxylic acid, spirohydantoin, and phenolic derivatives).
What was found
The abstract reports no quantitative experimental or clinical metrics. It outlines the biochemical cascade where hyperglycaemia leads to aldose reductase overexpression, sorbitol accumulation (osmotic stress), NADPH consumption, NAD+ reduction, NADH overproduction (reactive oxygen species and oxidative stress), and fructose overproduction, contributing to diabetic retinopathy, neuropathy, nephropathy, and non-alcoholic fatty liver disease.
Why it matters
It outlines the biological justification for developing aldose reductase inhibitors to prevent or mitigate microvascular and metabolic complications in diabetes.
Limits
The abstract provides a purely descriptive mechanistic overview lacking systematic literature search methodology, clinical trial evaluations, quantitative efficacy data, or safety profiles for the discussed inhibitors.
Cited by
- supports In diabetic retinopathies and nephropathies, excess intracellular glucose is diverted into the sorbitol pathway, where sorbitol accumulation creates an osmotic gradient causing hydropic degeneration and cell rupture.