ArticleScientific reports2019
Elastolytic activity of cysteine cathepsins K, S, and V promotes vascular calcification.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Proteolysis at the extracellular matrix interface: Molecular architects and regulators in health and disease.The FEBS journal · 2026Review
- Elastin calcification during the initial stage of vascular calcification in kl/kl mice is suppressed by the calcimimetic upacicalcet.Scientific reports · 2026Article
- Vasoconstriction-inhibiting factor: an endogenous inhibitor of vascular calcification as a calcimimetic of calcium-sensing receptor.Cardiovascular research · 2025Article
- Cathepsin S: molecular mechanisms in inflammatory and immunological processes.Frontiers in immunology · 2025Review
- Calcification of the elastic component: the impact on the cardiovascular system.Frontiers in cardiovascular medicine · 2025Review
- Vascular Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2024Review
- Excessive collagen fiber deposition in idiopathic scrotal calcinosis: a case report.BMC urology · 2024Article
- Fibroblasts' secretome from calcified and non-calcified dermis in Pseudoxanthoma elasticum differently contributes to elastin calcification.Communications biology · 2024Article
- Matrix metalloproteinase-3 joins a growing list of proteases that regulate vascular calcification.Cardiovascular research · 2024Article
- Molecular Mechanisms Underlying Vascular Remodeling in Hypertension.Reviews in cardiovascular medicine · 2024Review
- Elastin stabilization prevents impaired biomechanics in human pulmonary arteries and pulmonary hypertension in rats with left heart disease.Nature communications · 2023Article
- Role of elastic fiber degradation in disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine.Biomaterials research · 2023Review
- Kinetic Characterization of Cerium and Gallium Ions as Inhibitors of Cysteine Cathepsins L, K, and S.International journal of molecular sciences · 2022Article
- The Skeleton and Biomineralization Mechanism as Part of the Innate Immune System of Stony Corals.Frontiers in immunology · 2022Review
- Inappropriate cathepsin K secretion promotes its enzymatic activation driving heart and valve malformation.JCI insight · 2020Article
- Cathepsins in the Pathophysiology of Mucopolysaccharidoses: New Perspectives for Therapy.Cells · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Elastin plays an important role in maintaining blood vessel integrity. Proteolytic degradation of elastin in the vascular system promotes the development of atherosclerosis, including blood vessel calcification. Cysteine cathepsins have been implicated in this process, however, their role in disease progression and associated complications remains unclear. Here, we showed that the degradation of vascular elastin by cathepsins (Cat) K, S, and V directly stimulates the mineralization of elastin and that mineralized insoluble elastin fibers were ~25-30% more resistant to CatK, S, and V degradation when compared to native elastin. Energy dispersive X-ray spectroscopy investigations showed that insoluble elastin predigested by CatK, S, or V displayed an elemental percentage in calcium and phosphate up to 8-fold higher when compared to non-digested elastin. Cathepsin-generated elastin peptides increased the calcification of MOVAS-1 cells acting through the ERK1/2 pathway by 34-36%. We made similar observations when cathepsin-generated elastin peptides were added to ex vivo mouse aorta rings. Altogether, our data suggest that CatK-, S-, and V-mediated elastolysis directly accelerates the mineralization of the vascular matrix by the generation of nucleation points in the elastin matrix and indirectly by elastin-derived peptides stimulating the calcification by vascular smooth muscle cells. Both processes inversely protect against further extracellular matrix degradation.
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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.