Vascular calcification and cellular signaling pathways as potential therapeutic targets

Kang, Jeong-Hun; Kawano, Takahito; Murata, Masaharu; Toita, Riki

doi:10.1016/j.lfs.2023.122309

Cited by 8 publications

(3 citation statements)

References 249 publications

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“…The Wnt pathway plays diverse functions in embryonic development and adult homeostasis [ 94 ]. The activation of different Wnt signaling pathways promotes vascular calcification and valve sclerosis through different mechanisms [ 95 ]. The canonical Wnt/β-catenin functions by the binding of an extracellular Wnt ligand to a seven-pass transmembrane Frizzled (Fz) receptor and co-receptor low-density lipoprotein receptor-related protein (LRP5/6) activating β-catenin.…”

Section: Molecular Networking In Vascular Calcificationmentioning

confidence: 99%

“…Inside the nucleus, β-catenin forms a transcriptional complex with LEF-1/TCF DNA-binding transcription factors and induces the expression of specific target genes. In the case of pathological calcification, it upregulates markers of calcification, such as Runx2, BMPs, PPAR, or OPN [ 82 , 95 ]. On the other hand, the non-canonical Wnt signaling pathway stimulates pathological calcification through the Ror1/2 co-receptor and activates both branches, the Planar Cell Polarity pathway or PCP pathway and the Wnt/Ca 2+ pathway [ 96 , 97 ].…”

Section: Molecular Networking In Vascular Calcificationmentioning

confidence: 99%

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Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

Ortega,

De Leon-Oliva,

Gimeno-Longas

et al. 2024

Biomolecules

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Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification can occur in almost any soft tissue of the organism. The better studied is vascular calcification, where calcium salts can accumulate in the intima or medial layer or in aortic valves, and it is associated with higher mortality and cardiovascular events, including myocardial infarction, stroke, aortic and peripheral artery disease (PAD), and diabetes or chronic kidney disease (CKD), among others. The process involves an intricate interplay of different cellular components, endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and pericytes, concurrent with the activation of several signaling pathways, calcium, Wnt, BMP/Smad, and Notch, and the regulation by different molecular mediators, growth factors (GFs), osteogenic factors and matrix vesicles (MVs). In the present review, we aim to explore the cellular players, molecular pathways, biomarkers, and clinical treatment strategies associated with vascular calcification to provide a current and comprehensive overview of the topic.

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Section: Molecular Networking In Vascular Calcificationmentioning

confidence: 99%

Section: Molecular Networking In Vascular Calcificationmentioning

confidence: 99%

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

Ortega,

De Leon-Oliva,

Gimeno-Longas

et al. 2024

Biomolecules

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show abstract

“…Vascular calcification is a common complication of many diseases characterized by calcium deposition on the vessel wall, including diabetes, atherosclerosis, chronic kidney disease (CKD), and hypertension (1). Abnormal vascular calcification might impair vasomotor function and increase the risk of plaque rupture (2).…”

Section: Introductionmentioning

confidence: 99%

The emerging roles of irisin in vascular calcification

Wang,

Hu,

Pan

2024

Front. Endocrinol.

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Vascular calcification is a common accompanying pathological change in many chronic diseases, which is caused by calcium deposition in the blood vessel wall and leads to abnormal blood vessel function. With the progress of medical technology, the diagnosis rate of vascular calcification has explosively increased. However, due to its mechanism’s complexity, no effective drug can relieve or even reverse vascular calcification. Irisin is a myogenic cytokine regulating adipose tissue browning, energy metabolism, glucose metabolism, and other physiological processes. Previous studies have shown that irisin could serve as a predictor for vascular calcification, and protect against hypertension, diabetes, chronic kidney disease, and other risk factors for vascular calcification. In terms of mechanism, it improves vascular endothelial dysfunction and phenotypic transformation of vascular smooth muscle cells. All the above evidence suggests that irisin plays a predictive and protective role in vascular calcification. In this review, we summarize the association of irisin to the related risk factors for vascular calcification and mainly explore the role of irisin in vascular calcification.

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Endothelial cell Ass1 inhibits arteriosclerotic calcification in diabetes mellitus

Jiang,

Zhou,

Zhang

et al. 2024

Biomedicine & Pharmacotherapy

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Vascular calcification and cellular signaling pathways as potential therapeutic targets

Cited by 8 publications

References 249 publications

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

The emerging roles of irisin in vascular calcification

Endothelial cell Ass1 inhibits arteriosclerotic calcification in diabetes mellitus

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