ArticleMolecular medicine (Cambridge, Mass.)2017
Cathepsin L promotes Vascular Intimal Hyperplasia after Arterial Injury.
Article in Molecular medicine (Cambridge, Mass.), 2017. 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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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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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Macrophage-derived cathepsin L promotes epithelial-mesenchymal transition and M2 polarization in gastric cancer.World journal of gastroenterology · 2024Article
- Elevated Circulating Procathepsin L as a Potential Biomarker of Inflamm-aging.Medical hypotheses · 2024Article
- The many roles of cathepsins in restenosis.Heliyon · 2024Article
- Therapeutic potential of procathepsin L-inhibiting and progesterone-entrapping dimethyl-β-cyclodextrin nanoparticles in treating experimental sepsis.Frontiers in immunology · 2024Article
- Development of Procathepsin L (pCTS-L)-Inhibiting Lanosterol-Carrying Liposome Nanoparticles to Treat Lethal Sepsis.International journal of molecular sciences · 2023Article
- Identification of procathepsin L (pCTS-L)-neutralizing monoclonal antibodies to treat potentially lethal sepsis.Science advances · 2023Article
- Cathepsin L and acute ischemic stroke: A mini-review.Frontiers in stroke · 2022Review
- Exploring the mechanism of Danggui Buxue Decoction in regulating atherosclerotic disease network based on integrated pharmacological methods.Bioscience reports · 2021Article
- Targeting host cell proteases as a potential treatment strategy to limit the spread of SARS-CoV-2 in the respiratory tract.Pharmacology research & perspectives · 2021Review
- The HIV protease inhibitor Saquinavir attenuates sepsis-induced acute lung injury and promotes M2 macrophage polarization via targeting matrix metalloproteinase-9.Cell death & disease · 2021Article
- Caspase-11-Gasdermin D-Mediated Pyroptosis Is Involved in the Pathogenesis of Atherosclerosis.Frontiers in pharmacology · 2021Article
- Cathepsin L-selective inhibitors: A potentially promising treatment for COVID-19 patients.Pharmacology & therapeutics · 2020Review
- Hypertension, Thrombosis, Kidney Failure, and Diabetes: Is COVID-19 an Endothelial Disease? A Comprehensive Evaluation of Clinical and Basic Evidence.Journal of clinical medicine · 2020Review
- Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020Review
- Modulation of Cathepsin L Expression in the Coronary Arteries of Atherosclerotic Swine.The Journal of surgical research · 2019Article
- Cathepsin L expression in the carotid arteries of atherosclerotic swine.Archives of medical sciences. Atherosclerotic diseases · 2019Article
- A two-decade journey in identifying high mobility group box 1 (HMGB1) and procathepsin L (pCTS-L) as potential therapeutic targets for sepsis.Expert opinion on therapeutic targetsReview
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The inflammatory pathways that drive the development of intimal hyperplasia (IH) following arterial injury are not fully understood. We hypothesized that the lysosomal cysteine protease cathepsin L activates processes leading to IH after arterial injury. Using a mouse model of wire-induced carotid artery injury we showed that cathepsin L activity peaks at day 7 and remains elevated to 28 days. The genetic deletion of cathepsin L prevented IH and monocyte recruitment in the carotid wall. The injury-induced increases in cathepsin L mRNA and activity were mitigated in mice with myeloid-specific deletion of toll like receptor 4 (TLR4) or myeloid differentiation primary response gene 88 (MyD88). We further discovered that a HIV-protease inhibitor saquinavir (SQV), which is known to block recombinant mouse cathepsin L activity in vitro, prevented IH after arterial injury. SQV also suppressed LPS (TLR4 agonist) induced monocyte adhesion to endothelial monolayers. These findings establish cathepsin L as a critical regulator of the inflammation that leads to IH and that the TLR4- MyD88 pathway in myeloid lineages regulates cathepsin L expression in the vessel wall following wire injury. The FDA approved drug, SQV blocks IH though mechanisms that may include the suppression of cathepsin L.
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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.