ReviewJournal of biochemical and molecular toxicology2026
Iron-Sulfur Cluster Targeting: A Novel Perspective for Treating Alcohol-Related Lipid Metabolic Diseases.
Review in Journal of biochemical and molecular toxicology, 2026. 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.
- Iron-Sulfur Cluster Targeting: A Novel Perspective for Treating Alcohol-Related Lipid Metabolic Diseases.Journal of biochemical and molecular toxicology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Iron-sulfur (Fe-S) clusters are pivotal molecular cofactors bridging inorganic chemistry and organic life processes, with their tightly regulated biosynthesis and function underpinning cellular metabolic homeostasis. Chronic alcohol-induced metabolic stress impairs Fe-S cluster stability and biosynthesis via reactive oxygen species (ROS)-mediated oxidative damage and direct acetaldehyde toxicity, culminating in functional failure of this core cofactor. Current evidence is synthesized herein to delineate the hierarchical pathogenic cascade triggered by Fe-S cluster dysfunction. At the cellular level, Fe-S cluster depletion inactivates aconitase, driving citrate accumulation and redirecting carbon flux toward lipogenesis; concurrently, succinate dehydrogenase dysfunction causes succinate buildup, which epigenetically suppresses fatty acid oxidation. Impaired tRNA thiolation further compromises mitochondrial translational fidelity. Together, these defects precipitate an energy crisis and a self-perpetuating lipotoxicity-oxidative stress vicious cycle. At the systemic level, this metabolic dysregulation fuels disease progression from fatty liver and hyperlipidemia to atherosclerosis, mediated by enhanced hepatic VLDL secretion, reduced HDL levels, and oxidized LDL (Ox-LDL) formation. Furthermore, a hypothetical structural model for acetaldehyde-driven Fe-S cluster disintegration, grounded in organometallic chemistry principles. Collectively, this review highlights the central role of Fe-S clusters in alcohol-associated metabolic disorders and provides a novel theoretical framework for developing therapeutics targeting Fe-S cluster homeostasis.
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What Socratic 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 Socratic graph.