ArticleJournal of molecular and cellular cardiology2010
Polyol pathway impairs the function of SERCA and RyR in ischemic-reperfused rat hearts by increasing oxidative modifications of these proteins.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 46 citations in OpenAlex.
- Disrupted SR-Mitochondria Coupling Drives Ischemia-Reperfusion Vulnerability in the Middle-Aged Rat Heart.Biomedicines · 2026Article
- Stable oxidative posttranslational modifications alter the gating properties of RyR1.The Journal of general physiology · 2024Article
- The role of glycolytic metabolic pathways in cardiovascular disease and potential therapeutic approaches.Basic research in cardiology · 2023Review
- Nicotinamide restores tissue NAD+ and improves survival in rodent models of cardiac arrest.PloS one · 2023Article
- Identification of pharmacokinetic markers for safflower injection using a combination of system pharmacology, multicomponent pharmacokinetics, and quantitative proteomics study.Frontiers in pharmacology · 2022Article
- Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.Physiological research · 2021Review
- Inactivation of CysBritish journal of pharmacology · 2020Article
- Acute exposure to organic and inorganic sources of copper: Differential response in intestinal cell lines.Food science & nutrition · 2018Article
- Aldo-keto reductases-mediated cytotoxicity of 2-deoxyglucose: A novel anticancer mechanism.Cancer science · 2018Article
- Corticosteroids and aldose reductase inhibitor Epalrestat modulates cardiac action potential via Kvβ1.1 (AKR6A8) subunit of voltage-gated potassium channel.Molecular and cellular biochemistry · 2017Article
- Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes.Oxidative medicine and cellular longevity · 2017Review
- Dioxygen and Metabolism; Dangerous Liaisons in Cardiac Function and Disease.Frontiers in physiology · 2017Review
- The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited.Oxidative medicine and cellular longevity · 2016Review
- Unbreak my heart: targeting mitochondrial autophagy in diabetic cardiomyopathy.Antioxidants & redox signaling · 2015Review
- Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart.Heart failure reviews · 2015Review
- Oxidative stress and myocardial injury in the diabetic heart.The Journal of pathology · 2013Review
- Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion.Cardiovascular research · 2012Article
- A potential therapeutic role for aldose reductase inhibitors in the treatment of endotoxin-related inflammatory diseases.Expert opinion on investigational drugs · 2012Review
- Aldose reductase, oxidative stress, and diabetic mellitus.Frontiers in pharmacology · 2012 · on this mapArticle
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
A number of studies have shown that the polyol pathway, consisting of aldose reductase (AR) and sorbitol dehydrogenase (SDH), contributes to ischemia-reperfusion (I/R)-induced myocardial infarction due to depletion of ATP. In this report we show that the polyol pathway in I/R heart also contributes to the impairment of sacro/endoplasmic reticulum Ca(2+)-ATPase (SERCA) and ryanodine receptor (RyR), two key players in Ca(2+) signaling that regulate cardiac contraction. Rat hearts were isolated and retrogradely perfused with either Krebs' buffer containing 1 microM AR inhibitor, zopolrestat, or 200 nM SDH inhibitor, CP-170,711, and challenged by 30 min of regional ischemia and 45 min of reperfusion. We found that post-ischemic contractile function of the isolated perfused hearts was improved by pharmacological inhibition of the polyol pathway. I/R-induced contractile dysfunction is most likely due to impairment in Ca(2+) signaling and the activities of SERCA and RyR. All these abnormalities were significantly ameliorated by treatment with ARI or SDI. We showed that the polyol pathway activities increase the level of peroxynitrite, which enhances the tyrosine nitration of SERCA and irreversibly modifies it to form SERCAC674-SO(3)H. This leads to reduced level of S-glutathiolated SERCA, contributing to its inactivation. The polyol pathway activities also deplete the level of GSH, leading to decreased active RyR, the S-glutathiolated RyR. Thus, in I/R heart, inhibition of polyol pathway improved the function of SERCA and RyR by protecting them from irreversible oxidation.
Indexed as
Identifiers
What 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.