ArticleAmerican journal of translational research2016
TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions.MedComm · 2024Review
- Article
- Cytokine storm: behind the scenes of the collateral circulation after acute myocardial infarction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- LncRNA FGD5-AS1 reduces cardiomyocyte apoptosis and inflammation by modulating Akt and miR-223-3p expression.American journal of translational research · 2022Article
- Article
- Article
- Patients with Obstructive Sleep Apnea Have Altered Levels of Four Cytokines Associated with Cardiovascular and Kidney Disease, but Near Normal Levels with Airways Therapy.Nature and science of sleep · 2021Article
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Review
- Pre-treatment with a combination of Shenmai and Danshen injection protects cardiomyocytes against hypoxia/reoxygenation- and HExperimental and therapeutic medicine · 2019Article
- NETO2 promotes invasion and metastasis of gastric cancer cells via activation of PI3K/Akt/NF-κB/Snail axis and predicts outcome of the patients.Cell death & disease · 2019Article
- Apigenin suppresses the apoptosis of H9C2 rat cardiomyocytes subjected to myocardial ischemia‑reperfusion injury via upregulation of the PI3K/Akt pathway.Molecular medicine reports · 2018Article
- Protective effects ofJournal of thoracic disease · 2018Article
- Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.Trends in endocrinology and metabolism: TEM · 2017Review
- Article
- Kaempferide Protects against Myocardial Ischemia/Reperfusion Injury through Activation of the PI3K/Akt/GSK-3Mediators of inflammation · 2017Article
- miR-149-5p inhibits cell growth by regulating TWEAK/Fn14/PI3K/AKT pathway and predicts favorable survival in human osteosarcoma.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocyte apoptosis is a key determinant of cardiac recovery and prognosis of patients with acute myocardial infarction (AMI). Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of TNF superfamily, is a pro-inflammatory and pro-angiogenic cytokine implicated in physiological tissue regeneration and wound repair and is closely related to cardiac remodeling, dysfunction and fibrosis. However, the role of TWEAK and its receptor Fn14 in the cardiomyocyte apoptosis is still poorly understood. The present study aimed to investigate whether the TWEAK enhanced the cardiomyocyte apoptosis in AMI. The apoptosis of the cardiomyocyte cell line H9C2 was induced by hypoxia/reoxygenation. The apoptosis of H9C2 cells was evaluated by flow cytometry and caspase-3 activity assay under treatment with TWEAK at different concentrations. The phosphorylated signaling molecules and the expression involved in the surprising protection of TWEAK against the apoptosis with a dose-dependent manner (≥50 ng/ml). Furthermore, a rat myocardial ischemia and reperfusion (I/R) model was established by TWEAK preconditioning through injecting the TWEAK into the scar and border after ischemia immediately induced by ligating the left anterior descending coronary artery for 50 min and followed by different reperfusion times. The heart function was significantly improved in TWEAK preconditioning rats compared with controls as well as the infarct size was significantly reduced 21 days after reperfusion. Meanwhile, TWEAK protected the cardiac apoptosis by activation of cardioprotective signaling PI3K/AKT during I/R. Our findings suggest that TWEAK may represent a cardioprotective factor that inhibits the myocyte death of myocardial IRI.
Indexed as
Identifiers
27725864PMC5040682W2531066740What 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.