ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Fortilin reduces apoptosis in macrophages and promotes atherosclerosis.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.Communications biology · 2025Article
- High plasma levels of fortilin are associated with cardiovascular events in patients undergoing coronary angiography.Heart and vessels · 2025Article
- The multifaceted potential ofHeliyon · 2024Review
- Role of Translationally Controlled Tumor Protein (TCTP) in the Development of Hypertension and Related Diseases in Mouse Models.Biomedicines · 2022Review
- High Plasma Levels of Fortilin in Patients with Coronary Artery Disease.International journal of molecular sciences · 2022Article
- Expression and purification of a cleavable recombinant fortilin from Escherichia coli for structure activity studies.Protein expression and purification · 2022Article
- Fortilin inhibits p53, halts cardiomyocyte apoptosis, and protects the heart against heart failure.Cell death discovery · 2021Article
- Therapeutic potential of human umbilical cord mesenchymal stem cells on aortic atherosclerotic plaque in a high-fat diet rabbit model.Stem cell research & therapy · 2021Article
- Review
- Article
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- Ticagrelor induces paraoxonase-1 (PON1) and better protects hypercholesterolemic mice against atherosclerosis compared to clopidogrel.PloS one · 2019Article
- [Effects of simvastatin on aortic vascular endothelial cell apoptosis and Bcl-2 protein expression in a rat model of atherosclerosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Fortilin binds IRE1α and prevents ER stress from signaling apoptotic cell death.Nature communications · 2017Article
- Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice.Scientific reports · 2016Article
- Fortilin: A Potential Target for the Prevention and Treatment of Human Diseases.Advances in clinical chemistryReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis, a deadly disease insufficiently addressed by cholesterol-lowering drugs, needs new therapeutic strategies. Fortilin, a 172-amino acid multifunctional polypeptide, binds p53 and blocks its transcriptional activation of Bax, thereby exerting potent antiapoptotic activity. Although fortilin-overexpressing mice reportedly exhibit hypertension and accelerated atherosclerosis, it remains unknown if fortilin, not hypertension, facilitates atherosclerosis. Our objective was to test the hypothesis that fortilin in and of itself facilitates atherosclerosis by protecting macrophages against apoptosis. We generated fortilin-deficient (fortilin(+/-)) mice and wild-type counterparts (fortilin(+/+)) on a LDL receptor (Ldlr)(-/-) apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (Apobec1)(-/-) hypercholesterolemic genetic background, incubated them for 10 mo on a normal chow diet, and assessed the degree and extent of atherosclerosis. Despite similar blood pressure and lipid profiles, fortilin(+/-) mice exhibited significantly less atherosclerosis in their aortae than their fortilin(+/+) littermate controls. Quantitative immunostaining and flow cytometry analyses showed that the atherosclerotic lesions of fortilin(+/-) mice contained fewer macrophages than those of fortilin(+/+) mice. In addition, there were more apoptotic cells in the intima of fortilin(+/-) mice than in the intima of fortilin(+/+) mice. Furthermore, peritoneal macrophages from fortilin(+/-) mice expressed more Bax and underwent increased apoptosis, both at the baseline level and in response to oxidized LDL. Finally, hypercholesterolemic sera from Ldlr(-/-)Apobec1(-/-) mice induced fortilin in peritoneal macrophages more robustly than sera from control mice. In conclusion, fortilin, induced in the proatherosclerotic microenvironment in macrophages, protects macrophages against Bax-induced apoptosis, allows them to propagate, and accelerates atherosclerosis. Anti-fortilin therapy thus may represent a promising next generation antiatherosclerotic therapeutic strategy.
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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.