ArticleFrontiers in genetics2012
The molecular and physiological roles of ABCC6: more than meets the eye.
Article in Frontiers in genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- Aflibercept for choroidal neovascularizations secondary to pseudoxanthoma elasticum: a prospective study.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020Trial
- Pseudoxanthoma elasticum: cardiac findings in patients and Abcc6-deficient mouse model.PloS one · 2013Trial
- ABCC6 in Cellular Metabolic Homeostasis: Biochemical Links to Extracellular Nucleotide Signaling, Mitochondrial Stress, and Senescence.Cell biochemistry and biophysics · 2026Review
- Loss of ABCC6 in Human Mesenchymal Stem Cells Leads to Elevated Reactive Oxygen Species Formation and a Senescence-like Phenotype.Antioxidants (Basel, Switzerland) · 2026Article
- Pediatric ABCC6 deficiency: a genotypic and phenotypic analysis.Orphanet journal of rare diseases · 2025Review
- Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025Review
- ABCC6 Involvement in Cerebral Small Vessel Disease: Potential Mechanisms and Associations.Genes · 2025Review
- Investigation on ABCC6-Deficient Human Hepatocytes Generated by CRISPR-Cas9 Genome Editing.Cells · 2025Article
- Pseudoxanthoma elasticum, a difficult diagnostic in patient with dark skin.Skin health and disease · 2024Article
- Optic disc drusen: Dystrophic calcification, a potential target for treatment.Eye (London, England) · 2024Review
- Bone Marrow-Derived ABCC6 Is an Essential Regulator of Ectopic Calcification In Pseudoxanthoma Elasticum.The Journal of investigative dermatology · 2024Article
- The Purinergic Nature of Pseudoxanthoma Elasticum.Biology · 2024Review
- Choriocapillaris Flow Signal Impairment in Patients With Pseudoxanthoma Elasticum.Investigative ophthalmology & visual science · 2023Article
- Longitudinal assessment of vascular calcification in generalized arterial calcification of infancy.Pediatric radiology · 2022Review
- ABCC6 Knockdown Fuels Cell Proliferation by Regulating PPARα in Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- Review
- Ataluren-Promising Therapeutic Premature Termination Codon Readthrough Frontrunner.Pharmaceuticals (Basel, Switzerland) · 2021Review
- ABCC6, Pyrophosphate and Ectopic Calcification: Therapeutic Solutions.International journal of molecular sciences · 2021Review
- Structural and Functional Characterization of the ABCC6 Transporter in Hepatic Cells: Role on PXE, Cancer Therapy and Drug Resistance.International journal of molecular sciences · 2021Review
- ABCC6 deficiency promotes dyslipidemia and atherosclerosis.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 4 countries.
Funding
Abstract
Abnormal mineralization occurs in the context of several common conditions, including advanced age, diabetes, hypercholesterolemia, chronic renal failure, and certain genetic conditions. Metabolic, mechanical, infectious, and inflammatory injuries promote ectopic mineralization through overlapping yet distinct molecular mechanisms of initiation and progression. The ABCC6 protein is an ATP-dependent transporter primarily found in the plasma membrane of hepatocytes. ABCC6 exports unknown substrates from the liver presumably for systemic circulation. ABCC6 deficiency is the primary cause for chronic and acute forms of ectopic mineralization described in diseases such as pseudoxanthoma elasticum (PXE), β-thalassemia, and generalized arterial calcification of infancy (GACI) in humans and dystrophic cardiac calcification (DCC) in mice. These pathologies are characterized by mineralization of cardiovascular, ocular, and dermal tissues. PXE and to an extent GACI are caused by inactivating ABCC6 mutations, whereas the mineralization associated with β-thalassemia patients derives from a liver-specific change in ABCC6 expression. DCC is an acquired phenotype resulting from cardiovascular insults (ischemic injury or hyperlipidemia) and secondary to ABCC6 insufficiency. Abcc6-deficient mice develop ectopic calcifications similar to both the human PXE and mouse DCC phenotypes. The precise molecular and cellular mechanism linking deficient hepatic ABCC6 function to distal ectopic mineral deposition is not understood and has captured the attention of many research groups. Our previously published work along with that of others show that ABCC6 influences other modulators of calcification and that it plays a much greater physiological role than originally thought.
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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.