ArticleJournal of molecular and cellular cardiology2014
Ablation of Akt2 protects against lipopolysaccharide-induced cardiac dysfunction: role of Akt ubiquitination E3 ligase TRAF6.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 54 citations in OpenAlex.
- Pathological roles of ubiquitination and deubiquitination systems in sepsis-induced myocardial dysfunction.Biomolecules & biomedicine · 2025Review
- LIN28A-dependent lncRNA NEAT1 aggravates sepsis-induced acute respiratory distress syndrome through destabilizing ACE2 mRNA by RNA methylation.Journal of translational medicine · 2025Article
- Autophagy fine-tuning by angiotensin-(1-9) in cultured rat cardiomyocytes.Frontiers in cardiovascular medicine · 2025Article
- Novel biomarkers of preterm brain injury from blood transcriptome in sheep model of intrauterine asphyxia.Pediatric research · 2024Article
- Effect of L-carnitine in Ameliorating Lipopolysaccharide-Induced Cardiomyocyte Injury via MAPK Signaling.Molecular biotechnology · 2024Article
- PKM2 deficiency exacerbates gram-negative sepsis-induced cardiomyopathy via disrupting cardiac calcium homeostasis.Cell death discovery · 2022Article
- Cardiac-specific ITCH overexpression ameliorates septic cardiomyopathyJournal of molecular and cellular cardiology plus · 2022Article
- Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3.Yonsei medical journal · 2022Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress.Molecular medicine reports · 2021Article
- Cardamonin protects against lipopolysaccharide-induced myocardial contractile dysfunction in mice through Nrf2-regulated mechanism.Acta pharmacologica Sinica · 2021Article
- CD74 knockout protects against LPS-induced myocardial contractile dysfunction through AMPK-Skp2-SUV39H1-mediated demethylation of BCLB.British journal of pharmacology · 2020Article
- Metabolic syndrome diminishes insulin-induced Akt activation and causes a redistribution of Akt-interacting proteins in cardiomyocytes.PloS one · 2020Article
- Overexpression of miR-150-5p Alleviates Apoptosis in Sepsis-Induced Myocardial Depression.BioMed research international · 2020Article
- Accelerated Autophagy of Cecal Ligation and Puncture-Induced Myocardial Dysfunction and Its Correlation with Mammalian Target of Rapamycin Pathway in Rats.Chinese medical journal · 2018Article
- Tumor necrosis factor receptor-associated factor 6 as a nuclear factor kappa B-modulating therapeutic target in cardiovascular diseases: at the heart of it all.Translational research : the journal of laboratory and clinical medicine · 2018Review
- TRAF molecules in inflammation and inflammatory diseases.Current pharmacology reports · 2018Article
- 3-Bromo-4,5-Dihydroxybenzaldehyde Protects Against Myocardial Ischemia and Reperfusion Injury Through the Akt-PGC1α-Sirt3 Pathway.Frontiers in pharmacology · 2018Article
- Thioredoxin-1 attenuates sepsis-induced cardiomyopathy after cecal ligation and puncture in mice.The Journal of surgical research · 2017Article
- Proteasome dysfunction in cardiomyopathies.The Journal of physiology · 2017Review
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 at 3 institutions in 2 countries.
Funding
Abstract
Lipopolysaccharide (LPS), an essential component of the outer membrane of Gram-negative bacteria, plays a pivotal role in myocardial anomalies in sepsis. Recent evidence has depicted a role of Akt in LPS-induced cardiac sequelae although little information is available with regard to the contribution of Akt isoforms in the endotoxin-induced cardiac dysfunction. This study examined the effect of Akt2 knockout on LPS-induced myocardial contractile dysfunction and the underlying mechanism(s) with a focus on TNF receptor-associated factor 6 (TRAF6). Echocardiographic properties and cardiomyocyte contractile function [peak shortening (PS), maximal velocity of shortening/relengthening, time-to-PS, time-to-90% relengthening] were examined in wild-type and Akt2 knockout mice following LPS challenge (4mg/kg, 4h). LPS challenge enlarged LV end systolic diameter, reduced fractional shortening and cardiomyocyte contractile capacity, prolonged TR90, promoted apoptosis, upregulated caspase-3/-12, ubiquitin, and the ubiquitination E3 ligase TRAF6 as well as decreased mitochondrial membrane potential without affecting the levels of TNF-α, toll-like receptor 4 and the mitochondrial protein ALDH2. Although Akt2 knockout failed to affect myocardial function, apoptosis, and ubiquitination, it significantly attenuated or mitigated LPS-induced changes in cardiac contractile and mitochondrial function, apoptosis and ubiquitination but not TRAF6. LPS facilitated ubiquitination, phosphorylation of Akt, GSK3β and p38, the effect of which with the exception of p38 was ablated by Akt2 knockout. TRAF6 inhibitory peptide or RNA silencing significantly attenuated LPS-induced Akt2 ubiquitination, cardiac contractile anomalies and apoptosis. These data collectively suggested that TRAF6 may play a pivotal role in mediating LPS-induced cardiac injury via Akt2 ubiquitination.
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.