ArticleMediators of inflammation2014
TNF-like weak inducer of apoptosis aggravates left ventricular dysfunction after myocardial infarction in mice.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
The trial behind it
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Apoptotic markers and Dectin-1BMC cardiovascular disorders · 2026Article
- In Vitro Analysis of TWEAK/Fn14 Axis in the Blood-Brain Barrier Models during Oxygen-Glucose Deprivation and Reoxygenation.Molecular neurobiology · 2026Article
- Exploring the role of mitochondrial metabolism and immune infiltration in myocardial infarction: novel insights from bioinformatics and experimental validation.Frontiers in immunology · 2025Article
- TWEAK increases angiogenesis to promote diabetic skin wound healing by regulating Fn14/EGFR signaling.Journal of cosmetic dermatology · 2024Article
- Declined expressions of vast mitochondria-related genes represented by CYCS and transcription factor ESRRA in skeletal muscle aging.Bioengineered · 2021Article
- Higher levels of TWEAK and matrix metalloproteinase-3 during the acute phase of myocardial infarction are associated with adverse left ventricular remodeling.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2021Article
- Review
- TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14-NF-κB signaling pathway.Experimental and therapeutic medicine · 2018Article
- Effect of Aging on Mitochondrial Energetics in the Human Atria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Repair Injured Heart by Regulating Cardiac Regenerative Signals.Stem cells international · 2016Review
- PPARs: Protectors or Opponents of Myocardial Function?PPAR research · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTNF-like weak inducer of apoptosis (TWEAK) has recently been shown to be potentially involved in adverse cardiac remodeling. However, neither the exact role of TWEAK itself nor of its receptor Fn14 in this setting is known. AIM OF THE STUDY: To analyze the effects of sTWEAK on myocardial function and gene expression in response to experimental myocardial infarction in mice.
resultsTWEAK directly suppressed the expression of PGC-1α and genes of oxidative phosphorylation (OXPHOS) in cardiomyocytes. Systemic sTWEAK application after MI resulted in reduced left ventricular function and increased mortality without changes in interstitial fibrosis or infarct size. Molecular analysis revealed decreased phosphorylation of PI3K/Akt and ERK1/2 pathways associated with reduced expression of PGC-1α and PPARα. Likewise, expression of OXPHOS genes such as atp5O, cycs, cox5b, and ndufb5 was also reduced. Fn14-/- mice showed significantly improved left ventricular function and PGC-1α levels after MI compared to their respective WT littermates (Fn14+/+). Finally, inhibition of intrinsic TWEAK with anti-TWEAK antibodies resulted in improved left ventricular function and survival.
conclusionsTWEAK exerted maladaptive effects in mice after myocardial infarction most likely via direct effects on cardiomyocytes. Analysis of the potential mechanisms revealed that TWEAK reduced metabolic adaptations to increased cardiac workload by inhibition of PGC-1α.
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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.