Pseudoxanthoma elasticum, a prototype of heritable multisystem ectopic mineralization disorders, is caused by mutations in the ABCC6 gene encoding a putative efflux transporter, ABCC6. The phenotypic spectrum of pseudoxanthoma elasticum varies, and the correlation between genotype and phenotype has not been established. To identify genetic modifiers, we performed quantitative trait locus analysis in inbred mouse strains that carry the same hypomorphic allele in Abcc6 yet with highly variable ectopic mineralization phenotypes of pseudoxanthoma elasticum. Abcc6 was confirmed as a major determinant for ectopic mineralization in multiple tissues. Integrative analysis using functional genomics tools that included GeneWeaver, String, and Mouse Genome Informatics identified a total of nine additional candidate modifier genes that could influence the organ-specific ectopic mineralization phenotypes. Integration of the candidate genes into the existing ectopic mineralization gene network expands the current knowledge on the complexity of the network that, as a whole, governs ectopic mineralization in soft connective tissues.
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http://dx.doi.org/10.1016/j.jid.2019.04.023 | DOI Listing |
J Endocrinol Invest
December 2024
Department of Pharmacological and Biomolecular Sciences, Università Degli Studi Di Milano, 20133, Milan, Italy.
Background: Obesity, bone-related and cardiovascular diseases (CVD) are among the leading global health concerns. Growing evidence suggests that these conditions share common pathophysiological pathways and disease outcomes. PATHOGENETIC INTERACTIONS OF OBESITY, CVD AND BONE-RELATED DISEASES: Obesity is a well-established risk factor for atherosclerotic CVD (ASCVD), as dysfunctional ectopic adipose tissue may produce endocrine/paracrine hormones modulating metabolic processes and inflammation, predisposing to ASCVD.
View Article and Find Full Text PDFExpert Opin Pharmacother
December 2024
Department of Nephrology and Dialysis, past Drectoor, Alessandro Manzoni Hospital, ASST Lecco, Lecco, Italy.
Introduction: Hyperphosphatemia in advanced CKD often accompanies high PTH and FGF23 levels, impaired bone mineralization, ectopic calcifications, and increased cardiovascular risks. Novel treatments are now available to lower serum phosphorus effectively. However, safety, tolerability, and patient adherence must be evaluated to determine the best therapeutic option for hyperphosphatemia.
View Article and Find Full Text PDFHistochem Cell Biol
November 2024
Laboratory of Cellular and Microfluidic Technologies, Siberian State Medical University, 634050, Tomsk, Russian Federation.
Chelidonic acid (ChA) is small molecule capable of inducing the differentiation of mesenchymal stem cells (MSCs) into osteoblasts and the formation of mineralized bone matrix (MBM) both in vitro and in vivo. However, the molecular mechanisms underlying these effects are unknown. Therefore, in silico modelling of potential molecular targets of ChA was performed.
View Article and Find Full Text PDFMatrix Biol
December 2024
Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, PR China. Electronic address:
Atherosclerotic calcification often coincides with osteoporosis, suggesting a potential interplay between bone and vascular mineralization. Osteoblast-derived matrix vesicles (Ost-MVs), pivotal in bone mineralization, have emerged as potential contributors to ectopic vascular calcification. However, the precise role of Ost-MVs in vascular calcification and the underlying mechanisms remain elusive.
View Article and Find Full Text PDFLife Sci Alliance
January 2025
Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland
Brain calcification, the ectopic mineral deposits of calcium phosphate, is a frequent radiological finding and a diagnostic criterion for primary familial brain calcification. We previously showed that microglia curtail the growth of small vessel calcification via the triggering receptor expressed in myeloid 2 (TREM2) in the mouse model of primary familial brain calcification. Because boosting TREM2 function using activating antibodies has been shown to be beneficial in other disease conditions by aiding in microglial clearance of diverse pathologies, we investigated whether administration of a TREM2-activating antibody could mitigate vascular calcification in mice.
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