ArticleJournal of cellular and molecular medicine2014
Genetic deletion or TWEAK blocking antibody administration reduce atherosclerosis and enhance plaque stability in mice.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A potential fate decision landscape of the TWEAK/Fn14 axis on stem and progenitor cells: a systematic review.Stem cell research & therapy · 2022Pooled it
- Systematic Mendelian Randomization Exploring Druggable Genes for Hemorrhagic Strokes.Molecular neurobiology · 2025Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
- NIK Is a Mediator of Inflammation and Intimal Hyperplasia in Endothelial Denudation-Induced Vascular Injury.International journal of molecular sciences · 2024Article
- Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling.Frontiers in cell and developmental biology · 2023Review
- Validating human and mouse tissues commonly used in atherosclerosis research with coronary and aortic reference tissue: similarities but profound differences in disease initiation and plaque stability.JVS-vascular science · 2023Article
- Anti-TWEAK Antibody Alleviates Renal Interstitial Fibrosis by Increasing PGC-1α Expression in Lupus Nephritis.Journal of inflammation research · 2021Article
- Effects of influenza vaccination on the risk of cardiovascular and respiratory diseases and all-cause mortality.Ageing research reviews · 2020Review
- Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats.Odontology · 2020Article
- Review
- Changes in Soluble TWEAK Concentrations, but Not Those in Amyloid-β(1-40), Are Associated with a Decrease in Carotid Intima-Media Thickness after Bariatric Surgery in Obese Women.Obesity facts · 2020Article
- A major role of TWEAK/Fn14 axis as a therapeutic target for post-angioplasty restenosis.EBioMedicine · 2019Article
- Effect of influenza vaccine on tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in older adults.Vaccine · 2018Article
- The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors.Experimental and therapeutic medicine · 2017Article
- TWEAK blockade decreases atherosclerotic lesion size and progression through suppression of STAT1 signaling in diabetic mice.Scientific reports · 2017Article
- TWEAK favors phosphate-induced calcification of vascular smooth muscle cells through canonical and non-canonical activation of NFκB.Cell death & disease · 2016Article
- Cytokines: roles in atherosclerosis disease progression and potential therapeutic targets.Future medicinal chemistry · 2016Review
- Soluble TWEAK and Major Adverse Cardiovascular Events in Patients with CKD.Clinical journal of the American Society of Nephrology : CJASN · 2016Article
- Transition from identity to bioactivity-guided proteomics for biomarker discovery with focus on the PF2D platform.Proteomics. Clinical applications · 2016Review
- Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets.Cytokine & growth factor reviews · 2015Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical complications associated with atherosclerotic plaques arise from luminal obstruction due to plaque growth or destabilization leading to rupture. Tumour necrosis factor ligand superfamily member 12 (TNFSF12) also known as TNF-related weak inducer of apoptosis (TWEAK) is a proinflammatory cytokine that participates in atherosclerotic plaque development, but its role in plaque stability remains unclear. Using two different approaches, genetic deletion of TNFSF12 and treatment with a TWEAK blocking mAb in atherosclerosis-prone mice, we have analysed the effect of TWEAK inhibition on atherosclerotic plaques progression and stability. Mice lacking both TNFSF12 and Apolipoprotein E (TNFSF12(-/-) ApoE(-/-) ) exhibited a diminished atherosclerotic burden and lesion size in their aorta. Advanced atherosclerotic plaques of TNFSF12(-/-) ApoE(-/-) or anti-TWEAK treated mice exhibited an increase collagen/lipid and vascular smooth muscle cell/macrophage ratios compared with TNFSF12(+/+) ApoE(-/-) control mice, reflecting a more stable plaque phenotype. These changes are related with two different mechanisms, reduction of the inflammatory response (chemokines expression and secretion and nuclear factor kappa B activation) and decrease of metalloproteinase activity in atherosclerotic plaques of TNFSF12(-/-) ApoE(-/-) . A similar phenotype was observed with anti-TWEAK mAb treatment in TNFSF12(+/+) ApoE(-/-) mice. Brachiocephalic arteries were also examined since they exhibit additional features akin to human atherosclerotic plaques associated with instability and rupture. Features of greater plaque stability including augmented collagen/lipid ratio, reduced macrophage content, and less presence of lateral xanthomas, buried caps, medial erosion, intraplaque haemorrhage and calcium content were present in TNFSF12(-/-) ApoE(-/-) or anti-TWEAK treatment in TNFSF12(+/+) ApoE(-/-) mice. Overall, our data indicate that anti-TWEAK treatment has the capacity to diminish proinflamatory response associated with atherosclerotic plaque progression and to alter plaque morphology towards a stable phenotype.
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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.