Vascular calcification (VC) is an independent cardiovascular event and also a complication commonly found in chronic kidney disease (CKD) and diabetic patients. The mechanisms underpinning pathophysiology of VC is yet to be fully understood. Nevertheless, certain processes are generally believed to participate in its onset and progression. VC pathology is characterized by disequilibrium in the amount of natural inhibitors and active inducers of VC process. The imbalance may favor ectopic deposition of calcium-phosphate in form of hydroxyapatite in media or intima tunica compartments of blood vessels. This eventually could trigger phenotypic switch of smooth muscle cells to osteoblasts related cells. Thus, VSMC phenotypic trans-differentiation is currently considered as one of the hallmarks of VC. At the moment, there is no approved treatment. Fibroblast growth factors (FGFs) are a protein family that participates in varieties of biological processes. More recently, FGF21 seems to be gaining more attention with recent findings showing its anti-calcifying efficacy. In this review, the aim is to point out specific processes involved in VC and also to highlight the participation of FGF21 in the pathology of vascular calcification.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.vph.2019.106636DOI Listing

Publication Analysis

Top Keywords

vascular calcification
12
fibroblast growth
8
pathology vascular
8
growth factor
4
factor review
4
review participation
4
participation vascular
4
calcification pathology
4
calcification independent
4
independent cardiovascular
4

Similar Publications

Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Vanderbilt Memory and Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA.

Background: In humans, larger artery stiffening is associated with increased tau phosphorylation and neurodegeneration. However, because arterial stiffness often co-occurs with other age-related conditions like hypertension, atherosclerosis, and diabetes, it is nearly impossible to distill the underlying mechanisms specifically linking arterial stiffening to abnormal brain function. We leveraged a surgical mouse model of larger artery stiffening and used it concurrently with a transgenic Alzheimer's disease (AD) mouse model of tau pathology to investigate the impact of larger artery stiffening on cognition.

View Article and Find Full Text PDF

Vertebral fracture assessment (VFA) images from bone density machines enable the automated machine learning assessment of abdominal aortic calcification (ML-AAC), a marker of cardiovascular disease (CVD) risk. The objective of this study was to describe the risk of a major adverse cardiovascular event (MACE, from linked health records) in patients attending routine bone mineral density (BMD) testing and meeting specific criteria based on age, BMD, height loss, or glucocorticoid use have a VFA in the Manitoba Bone Mineral Density Registry. The cohort included 10 250 individuals (mean 75.

View Article and Find Full Text PDF

Background: Mitral annular calcification (MAC) is characterized by severe calcification of mitral annulus and might be associated with both mitral regurgitation and stenosis. It is technically challenging for both surgical and percutaneous approach and is burdened by high mortality.

Case Summary: The present case report describes a complex case of mitral steno-insufficiency (baseline transvalvular gradient = 5 mmHg, effective regurgitant orifice area 0.

View Article and Find Full Text PDF

Deficiency of Sox7 leads to congenital aortic stenosis via abnormal valve remodeling.

J Mol Cell Cardiol

December 2024

Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China. Electronic address:

Abnormal valve development is the most common congenital heart malformation. The transcription factor Sox7 plays a critical role in the development of vascular and cardiac septation. However, it remains unclear whether Sox7 is required for heart valve development.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!