ArticleHypertension (Dallas, Tex. : 1979)2014
Cathepsin K activity controls injury-related vascular repair in mice.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Relationship between cathepsin K and extracellular matrix dynamics: a comprehensive review.Frontiers in oncology · 2026Review
- CD8FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Molecular Mechanisms Underlying Vascular Remodeling in Hypertension.Reviews in cardiovascular medicine · 2024Review
- Overview of multifunctional cysteinyl cathepsins in atherosclerosis-based cardiovascular disease: from insights into molecular functions to clinical implications.Cell & bioscience · 2023Review
- Co-infection of TYLCV and ToCV increases cathepsin B and promotes ToCV transmission byFrontiers in microbiology · 2023Article
- Cathepsin K: A Versatile Potential Biomarker and Therapeutic Target for Various Cancers.Current oncology (Toronto, Ont.) · 2022Review
- Dipeptidyl peptidase-4 inhibition prevents lung injury in mice under chronic stress via the modulation of oxidative stress and inflammation.Experimental animals · 2021Article
- MED1 Deficiency in Macrophages Accelerates Intimal Hyperplasia via ROS Generation and Inflammation.Oxidative medicine and cellular longevity · 2021Article
- Cysteine cathepsins are altered by flow within an engineeredAPL bioengineering · 2020Article
- Cathepsin K Deficiency Impaired Ischemia-Induced Neovascularization in Aged Mice.Stem cells international · 2020Article
- PLF-1 (Proliferin-1) Modulates Smooth Muscle Cell Proliferation and Development of Experimental Intimal Hyperplasia.Journal of the American Heart Association · 2019Article
- Cathepsin S Deficiency Mitigated Chronic Stress-Related Neointimal Hyperplasia in Mice.Journal of the American Heart Association · 2019Article
- Lycopene restores the effect of ischemic postconditioning on myocardial ischemia‑reperfusion injury in hypercholesterolemic rats.International journal of molecular medicine · 2019Article
- HDAC6 is associated with the formation of aortic dissection in human.Molecular medicine (Cambridge, Mass.) · 2019Article
- Endogenous reduction of miR-185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K.Journal of cellular and molecular medicine · 2019Article
- Human cathepsins K, L, and S: Related proteases, but unique fibrinolytic activity.Biochimica et biophysica acta. General subjects · 2018Article
- l-Homocysteine-induced cathepsin V mediates the vascular endothelial inflammation in hyperhomocysteinaemia.British journal of pharmacology · 2018Article
- Cathepsin K activity controls cardiotoxin-induced skeletal muscle repair in mice.Journal of cachexia, sarcopenia and muscle · 2018Article
- Cysteine Protease Cathepsins in Atherosclerotic Cardiovascular Diseases.Journal of atherosclerosis and thrombosis · 2018Review
- Microbiota control acute arterial inflammation and neointimal hyperplasia development after arterial injury.PloS one · 2018Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Cathepsin K (CatK) is one of the most potent mammalian collagenases. We showed previously the increased expression of CatK in human and animal atherosclerotic lesions. Here, we hypothesized that ablation of CatK mitigates injury-induced neointimal hyperplasia. Male wild-type (CatK(+/+)) and CatK-deficient (CatK(-/-)) mice underwent ligation or a combination of ligation and polyethylene cuff-replacement injuries to the right common carotid artery just proximal to its bifurcation, and they were then processed for morphological and biochemical studies at specific time points. On operative day 28, CatK(-/-) significantly reduced neointimal formation and neovessel formation in both single- and combination-injured arteries compared with the Cat K(+/+) mice. At early time points, CatK(-/-) reduced the lesion macrophage contents and medial smooth muscle cell proliferation, the mRNA levels of monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, chemokine ligand-12, and the gelatinolytic activity related to matrix metalloproteinase-2/-9. An aorta-explant assay revealed that smooth muscle cell movement was impaired in the CatK(-/-) mice compared with the CatK(+/+) mice. In addition, the smooth muscle cells and macrophages from CatK(-/-) mice had less invasive ability through a reconstituted basement membrane barrier. This vasculoprotective effect was mimicked by Cat inhibition with trans-epoxysuccinyl-L-leucylamido-{4-guanidino} butane (E64d). These results demonstrate an essential role of CatK in neointimal lesion formation in response to injury, possibly via the reduction of toll-like receptor-2/-4-mediated inflammation and smooth muscle cell proliferation, suggesting a novel therapeutic strategy for the control of endovascular treatment-related restenosis by regulating CatK activity.
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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.