Rac1 mediates cadherin-11 induced cellular pathogenic processes in aortic valve calcification

Vaidya, Kiran A.; Donnelly, Matthew P.; Mahmut, Ablajan; Jang, Jae Woong; Gee, Terence W.; Aibo, Marine-Ayan Ibrahim; Bossong, Robert; Hall, C.M.; Samb, Sanjay; Chen, Jonathan; Butcher, Jonathan T.

doi:10.1016/j.carpath.2022.107414

Cited by 4 publications

(1 citation statement)

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“…Among these promoters, cadherin-11 (Cad11) is a cell–cell adhesion protein related to inflammation in rheumatoid arthritis. Cad11 induces aortic valve calcification through Rac1, and its overexpression leads to the upregulation of RhoA and Sox9 and extracellular matrix remodeling [ 120 , 121 ]. Calcific nodule morphogenesis by valvular myofibroblasts requires robust cell–cell connections regulated by Cad11 [ 122 , 123 ].…”

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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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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