ArticleChemico-biological interactions2009
Aldose reductase decreases endoplasmic reticulum stress in ischemic hearts.
Article in Chemico-biological interactions, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- In vitro evaluation of the reductive carbonyl idarubicin metabolism to evaluate inhibitors of the formation of cardiotoxic idarubicinol via carbonyl and aldo-keto reductases.Archives of toxicology · 2024Article
- Effects of intracardiac delivery of aldehyde dehydrogenase 2 gene in myocardial salvage.Gene therapy · 2023Article
- Electrophilic Aldehyde 4-Hydroxy-2-Nonenal Mediated Signaling and Mitochondrial Dysfunction.Biomolecules · 2022Review
- Diabetic Aldehyde Dehydrogenase 2 Mutant (ALDH2*2) Mice Are More Susceptible to Cardiac Ischemic-Reperfusion Injury Due to 4-Hydroxy-2-Nonenal Induced Coronary Endothelial Cell Damage.Journal of the American Heart Association · 2021Article
- Cardiospecific Overexpression of ATPGD1 (Carnosine Synthase) Increases Histidine Dipeptide Levels and Prevents Myocardial Ischemia Reperfusion Injury.Journal of the American Heart Association · 2020Article
- Transduced Tat-aldose Reductase Protects Hippocampal Neuronal Cells against Oxidative Stress-induced Damage.Experimental neurobiology · 2019Article
- Aldose reductase inhibition enhances lens regeneration in mice.Chemico-biological interactions · 2019Article
- Carnosine protects cardiac myocytes against lipid peroxidation products.Amino acids · 2019Article
- AKR1B1 Upregulation Contributes to Neuroinflammation and Astrocytes Proliferation by Regulating the Energy Metabolism in Rat Spinal Cord Injury.Neurochemical research · 2018Review
- Deficiency of aldose reductase exacerbates early pressure overload-induced cardiac dysfunction and autophagy in mice.Journal of molecular and cellular cardiology · 2018Article
- Biomarkers of Chronic Acrolein Inhalation Exposure in Mice: Implications for Tobacco Product-Induced Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Natural formulas and the nature of formulas: Exploring potential therapeutic targets based on traditional Chinese herbal formulas.PloS one · 2017Article
- 4-Hydroxy-nonenal-A Bioactive Lipid Peroxidation Product.Biomolecules · 2015Review
- Glutathione S-transferase P protects against cyclophosphamide-induced cardiotoxicity in mice.Toxicology and applied pharmacology · 2015Article
- Molecular mechanisms of acrolein toxicity: relevance to human disease.Toxicological sciences : an official journal of the Society of Toxicology · 2015Review
- Lipid peroxidation generates biologically active phospholipids including oxidatively N-modified phospholipids.Chemistry and physics of lipids · 2014Review
- Total ginsenosides of Radix Ginseng modulates tricarboxylic acid cycle protein expression to enhance cardiac energy metabolism in ischemic rat heart tissues.Molecules (Basel, Switzerland) · 2012Article
- Transcriptional analysis implicates endoplasmic reticulum stress in bovine spongiform encephalopathy.PloS one · 2010Article
- Postischemic deactivation of cardiac aldose reductase: role of glutathione S-transferase P and glutaredoxin in regeneration of reduced thiols from sulfenic acids.The Journal of biological chemistry · 2010Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Aldose reductase (AR) is a multi-functional AKR (AKR1B1) that catalyzes the reduction of a wide range of endogenous and xenobiotic aldehydes and their glutathione conjugates with high efficiency. Previous studies from our laboratory show that AR protects against myocardial ischemia-reperfusion injury, however, the mechanisms by which it confers cardioprotection remain unknown. Because AR metabolizes aldehydes generated from lipid peroxidation, we tested the hypothesis that it protects against ischemic injury by preventing ER stress induced by excessive accumulation of aldehyde-modified proteins in the ischemic heart. In cell culture experiments, exposure to model lipid peroxidation aldehydes-4-hydroxy-trans-2-nonenal (HNE), 1-palmitoyl-2-oxovaleroyl phosphatidylcholine (POVPC) or acrolein led to an increase in the phosphorylation of ER stress markers PERK and eIF2-alpha and an increase in ATF3. The reduced metabolite of POVPC 1-palmitoyl-2-hydroxyvaleroyl phosphatidylcholine (PHVPC) was unable to stimulate JNK phosphorylation. No increase in phospho-eIF2-alpha, ATF3 or phospho-PERK was observed in cells treated with the reduced HNE metabolite 1,4-dihydroxynonenol (DHN). Lysates prepared from isolated perfused mouse hearts subjected to 15 min of global ischemia followed by 30 min of reperfusion ex vivo showed greater phosphorylation of PERK and eIF2-alpha than hearts subjected to aerobic perfusion alone. Ischemia-induced increases in phospho-PERK and phospho-eIF2-alpha were diminished in the hearts of cardiomyocyte-specific transgenic mice overexpressing the AR transgene. These observations support the notion that by removing aldehydic products of lipid peroxidation, AR decreases ischemia-reperfusion injury by diminishing ER stress.
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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.