ArticleInternational archives of medicine2010
LDLR-Gene therapy for familial hypercholesterolaemia: problems, progress, and perspectives.
Article in International archives of medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 57 citations in OpenAlex.
- High-capacity adenoviral vector-mediated expression of an LDLR/transferrin chimeric protein in muscle reduces atherosclerosis in LdlrMolecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- A de novo LDLR mutation in severe familial hypercholesterolemia: case report, functional characterization, and a personalized gene correction strategy exploration.Frontiers in cardiovascular medicine · 2026Article
- Novel Gene-Correction-Based Therapeutic Modalities for Monogenic Liver Disorders.Bioengineering (Basel, Switzerland) · 2022Review
- Gene Therapy for Progressive Familial Intrahepatic Cholestasis: Current Progress and Future Prospects.International journal of molecular sciences · 2020Review
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- Article
- Helper-dependent adenovirus-mediated gene transfer of a secreted LDL receptor/transferrin chimeric protein reduces aortic atherosclerosis in LDL receptor-deficient mice.Gene therapy · 2019Article
- A Rare Missense Mutation and a Polymorphism with High Frequency inAdvanced biomedical research · 2018Article
- Efficient Generation of Somatic Cell Nuclear Transfer-Competent Porcine Cells with Mutated Alleles at Multiple Target Loci by Using CRISPR/Cas9 Combined with Targeted Toxin-Based Selection System.International journal of molecular sciences · 2017Article
- MicroRNA: a connecting road between apoptosis and cholesterol metabolism.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Recent Developments in Gene Therapy for Homozygous Familial Hypercholesterolemia.Current atherosclerosis reports · 2016Review
- Release of Vesicular Stomatitis Virus Spike Protein G-Pseudotyped Lentivirus from the Host Cell Is Impaired upon Low-Density Lipoprotein Receptor Overexpression.Journal of virology · 2015Article
- Management of patients with familial hypercholesterolaemia.Nature reviews. Cardiology · 2015Review
- Identification and Treatment of Patients with Homozygous Familial Hypercholesterolaemia: Information and Recommendations from a Middle East Advisory Panel.Current vascular pharmacology · 2015Article
- Familial hypercholesterolemia: A review.Annals of pediatric cardiology · 2014Review
- Identification of a novel nonsense variant c.1332dup, p.(D445*) in the LDLR gene that causes familial hypercholesterolemia.Human genome variation · 2014Article
- Genetic polymorphisms in LDLR, APOB, PCSK9 and other lipid related genes associated with familial hypercholesterolemia in Malaysia.PloS one · 2013Article
- HDL, Atherosclerosis, and Emerging Therapies.Cholesterol · 2013Article
- Regulation and deregulation of cholesterol homeostasis: The liver as a metabolic "power station".World journal of hepatology · 2012Article
- Role of lipid apheresis in changing times.Clinical research in cardiology supplements · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary artery diseases (CAD) inflict a heavy economical and social burden on most populations and contribute significantly to their morbidity and mortality rates. Low-density lipoprotein receptor (LDLR) associated familial hypercholesterolemia (FH) is the most frequent Mendelian disorder and is a major risk factor for the development of CAD. To date there is no cure for FH. The primary goal of clinical management is to control hypercholesterolaemia in order to decrease the risk of atherosclerosis and to prevent CAD. Permanent phenotypic correction with single administration of a gene therapeutic vector is a goal still needing to be achieved. The first ex vivo clinical trial of gene therapy in FH was conducted nearly 18 years ago. Patients who had inherited LDLR gene mutations were subjected to an aggressive surgical intervention involving partial hepatectomy to obtain the patient's own hepatocytes for ex vivo gene transfer with a replication deficient LDLR-retroviral vector. After successful re-infusion of transduced cells through a catheter placed in the inferior mesenteric vein at the time of liver resection, only low-level expression of the transferred LDLR gene was observed in the five patients enrolled in the trial. In contrast, full reversal of hypercholesterolaemia was later demonstrated in in vivo preclinical studies using LDLR-adenovirus mediated gene transfer. However, the high efficiency of cell division independent gene transfer by adenovirus vectors is limited by their short-term persistence due to episomal maintenance and the cytotoxicity of these highly immunogenic viruses. Novel long-term persisting vectors derived from adeno-associated viruses and lentiviruses, are now available and investigations are underway to determine their safety and efficiency in preparation for clinical application for a variety of diseases. Several novel non-viral based therapies have also been developed recently to lower LDL-C serum levels in FH patients. This article reviews the progress made in the 18 years since the first clinical trial for gene therapy of FH, with emphasis on the development, design, performance and limitations of viral based gene transfer vectors used in studies to ameliorate the effects of LDLR deficiency.
Identifiers
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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.