ArticleArteriosclerosis, thrombosis, and vascular biology2012
Cathepsin K deficiency reduces elastase perfusion-induced abdominal aortic aneurysms in mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 97 citations in OpenAlex.
- A clinical evaluation of statin pleiotropy: statins selectively and dose-dependently reduce vascular inflammation.PloS one · 2013Trial
- Plasma cathepsin S and cystatin C levels and risk of abdominal aortic aneurysm: a randomized population-based study.PloS one · 2012 · on this mapTrial
- Circulating elastin fragments drive systemic aging: Where do pro-aging elastin fragments come from? A mini-review.Mechanisms of ageing and development · 2026Review
- Review
- Cathepsin K inhibition promotes efficient differentiation of human embryonic stem cells to mature cardiomyocytes by mediating glucolipid metabolism and cellular energy homeostasis.Stem cell research & therapy · 2025Article
- Review
- Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023Review
- Overview of multifunctional cysteinyl cathepsins in atherosclerosis-based cardiovascular disease: from insights into molecular functions to clinical implications.Cell & bioscience · 2023Review
- Cysteine Cathepsins as Therapeutic Targets in Immune Regulation and Immune Disorders.Biomedicines · 2023Review
- Role of Extracellular Matrix and Inflammation in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2022Review
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- AAA Revisited: A Comprehensive Review of Risk Factors, Management, and Hallmarks of Pathogenesis.Biomedicines · 2022Review
- Nanoparticle-Mediated Delivery of Pitavastatin to Monocytes/Macrophages Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in ApoeJournal of atherosclerosis and thrombosis · 2022Article
- Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Single-cell RNA sequencing reveals the cellular heterogeneity of aneurysmal infrarenal abdominal aorta.Cardiovascular research · 2021Article
- KLF11 protects against abdominal aortic aneurysm through inhibition of endothelial cell dysfunction.JCI insight · 2021Article
- Translating mouse models of abdominal aortic aneurysm to the translational needs of vascular surgery.JVS-vascular science · 2021Review
- Genetic and Epigenetic Mechanisms Underlying Vascular Smooth Muscle Cell Phenotypic Modulation in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2020Review
- Assessing the targeting and fate of cathepsin k antibody-modified nanoparticles in a rat abdominal aortic aneurysm model.Acta biomaterialia · 2020Article
- Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveCathepsin K (CatK) is one of the most potent mammalian elastases. We have previously shown increased expression of CatK in human abdominal aortic aneurysm (AAA) lesions. Whether this protease participates directly in AAA formation, however, remains unknown. METHODS AND
resultsMouse experimental AAA was induced with aortic perfusion of a porcine pancreatic elastase. Using this experimental model, we demonstrated that absence of CatK prevented AAA formation in mice 14 days postperfusion. CatK deficiency significantly reduced lesion CD4(+) T-cell content, total lesion and medial cell proliferation and apoptosis, medial smooth muscle cell (SMC) loss, elastinolytic CatL and CatS expression, and elastin fragmentation, but it did not affect AAA lesion Mac-3(+) macrophage accumulation or CD31(+) microvessel numbers. In vitro studies revealed that CatK contributed importantly to CD4(+) T-cell proliferation, SMC apoptosis, and other cysteinyl cathepsin and matrix metalloproteinase expression and activities in SMCs and endothelial cells but played negligible roles in microvessel growth and monocyte migration. AAA lesions from CatK-deficient mice showed reduced elastinolytic cathepsin activities compared with those from wild-type control mice.
conclusionsThis study demonstrates that CatK plays an essential role in AAA formation by promoting T-cell proliferation, vascular SMC apoptosis, and elastin degradation and by affecting vascular cell protease expression and activities.
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Registered trials
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