ArticleAntioxidants & redox signaling2011
Activation of Akt rescues endoplasmic reticulum stress-impaired murine cardiac contractile function via glycogen synthase kinase-3β-mediated suppression of mitochondrial permeation pore opening.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 35 papers.
What it found
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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.
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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.
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Who cites it
35 citing papers in PubMed, 72 citations in OpenAlex.
- RETRACTION: Short-Chain Fatty Acid Propionate Alleviates Akt2 Knockout-Induced Myocardial Contractile Dysfunction.Journal of diabetes research · 2025Article
- Mitochondrial aldehyde dehydrogenase rescues against diabetic cardiomyopathy through GSK3β-mediated preservation of mitochondrial integrity and Parkin-mediated mitophagy.Journal of molecular cell biology · 2024Article
- Non-coding RNA mediates endoplasmic reticulum stress-induced apoptosis in heart disease.Heliyon · 2023Review
- Protective Role of Hepassocin against Hepatic Endoplasmic Reticulum Stress in Mice.International journal of molecular sciences · 2022Article
- Retraction Note: Mitochondrial aldehyde dehydrogenase (ALDH2) protects against streptozotocin-induced diabetic cardiomyopathy: role of GSK3β and mitochondrial function.BMC medicine · 2022Article
- Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Mitochondrial aldehyde dehydrogenase (ALDH2) rescues cardiac contractile dysfunction in an APP/PS1 murine model of Alzheimer's disease via inhibition of ACSL4-dependent ferroptosis.Acta pharmacologica Sinica · 2022Article
- Cardamonin protects against lipopolysaccharide-induced myocardial contractile dysfunction in mice through Nrf2-regulated mechanism.Acta pharmacologica Sinica · 2021Article
- Apelin ameliorated acute heart failure via inhibiting endoplasmic reticulum stress in rabbits.Amino acids · 2021Article
- Does Transient Receptor Potential Vanilloid Type 1 Alleviate or Aggravate Pathological Myocardial Hypertrophy?Frontiers in pharmacology · 2021Review
- Mitochondrial CaActa pharmacologica Sinica · 2020Review
- CD74 knockout protects against LPS-induced myocardial contractile dysfunction through AMPK-Skp2-SUV39H1-mediated demethylation of BCLB.British journal of pharmacology · 2020Article
- Left ventricular response in the transition from hypertrophy to failure recapitulates distinct roles of Akt, β-arrestin-2, and CaMKII in mice with aortic regurgitation.Annals of translational medicine · 2020Article
- Metabolic syndrome diminishes insulin-induced Akt activation and causes a redistribution of Akt-interacting proteins in cardiomyocytes.PloS one · 2020Article
- SGK1 Attenuates Oxidative Stress-Induced Renal Tubular Epithelial Cell Injury by Regulating Mitochondrial Function.Oxidative medicine and cellular longevity · 2019Article
- SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.Cell death and differentiation · 2017Article
- Aerobic exercise training rescues cardiac protein quality control and blunts endoplasmic reticulum stress in heart failure rats.Journal of cellular and molecular medicine · 2016Article
- Salvianolic acid B protects against doxorubicin induced cardiac dysfunctionToxicology research · 2016Article
- Upregulated ATF6 contributes to chronic intermittent hypoxia-afforded protection against myocardial ischemia/reperfusion injury.International journal of molecular medicine · 2016Article
- Article
Corrections and comments
- Retraction · 2023-04-18Concerns/Issues about Data · Duplication of/in Image · Investigation by Company/Institution · Unreliable Results and/or Conclusions · · Jun Ren has institutional finding of misconduct;
- Retracted
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
aimsThe present study was designed to examine the impact of chronic Akt activation on endoplasmic reticulum (ER) stress-induced cardiac mechanical anomalies, if any, and the underlying mechanism involved.
resultsWild-type and transgenic mice with cardiac-specific overexpression of the active mutant of Akt (Myr-Akt) were subjected to the ER stress inducer tunicamycin (1 or 3 mg/kg). ER stress led to compromised echocardiographic (elevated left ventricular end-systolic diameter and reduced fractional shortening) and cardiomyocyte contractile function, intracellular Ca(2+) mishandling, and cell survival in wild-type mice associated with mitochondrial damage. In vitro ER stress induction in murine cardiomyocytes upregulated the ER stress proteins Gadd153, GRP78, and phospho-eIF2α, and promoted reactive oxygen species production, carbonyl formation, apoptosis, mitochondrial membrane potential loss, and mitochondrial permeation pore (mPTP) opening associated with overtly impaired cardiomyocyte contractile and intracellular Ca(2+) properties. Interestingly, these anomalies were mitigated by chronic Akt activation or the ER chaperon tauroursodeoxycholic acid (TUDCA). Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3β (GSK3β) (leading to activation of GSK3β), the effect of which was abrogated by Akt activation and TUDCA. The ER stress-induced cardiomyocyte contractile and mitochondrial anomalies were obliterated by the mPTP inhibitor cyclosporin A, GSK3β inhibitor SB216763, and ER stress inhibitor TUDCA. INNOVATION: This research reported the direct relationship between ER stress and cardiomyocyte contractile and mitochondrial anomalies for the first time.
conclusionTaken together, these data suggest that ER stress may compromise cardiac contractile and intracellular Ca(2+) properties, possibly through the Akt/GSK3β-dependent impairment of mitochondrial integrity.
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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.