ArticlePloS one2024
Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway.
Article in PloS one, 2024. 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, 16 citations in OpenAlex.
- Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting pyroptosis in atherosclerosis: emerging pharmacologic strategies and natural compound-based therapeutics-a narrative review.International journal of clinical pharmacy · 2026Review
- Delving into pyroptosis in atherosclerosis: role, mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Identification of immune-mediated aging genes associated with cervical spondylosis through single-cell eQTL Mendelian randomization.Frontiers in immunology · 2026Article
- Cathepsin B ablation alleviates VSMC phenotypic switching by modulating alternative macrophage polarization through the NLRP3 signaling pathway.Frontiers in cardiovascular medicine · 2026Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Atherosclerosis-induced arterial erectile dysfunction: pathogenesis, diagnosis, and therapeutic strategies.Translational andrology and urology · 2025Review
- The molecular mechanism by which CTSB degrades FPN to disrupt macrophage iron homeostasis and promote the progression of atherosclerosis.Molecular and cellular biochemistry · 2025Article
- Macrophages release neuraminidase and cleaved calreticulin for programmed cell removal.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting cholesterol-driven pyroptosis: a promising strategy for the prevention and treatment of atherosclerosis.Molecular biology reports · 2025Review
- TRIM21 Promotes Endothelial Cell Activation via Accelerating SOCS3 Ubiquitination Degradation in Atherosclerosis.Cardiovascular toxicology · 2025Article
- Identification of critical endoplasmic reticulum stress-related genes in advanced atherosclerotic plaque.Scientific reports · 2025Article
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- The relationship between programmed cell death and vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- Pyroptosis in Endothelial Cells and Extracellular Vesicle Release in Atherosclerosis via NF-κB-Caspase-4/5-GSDM-D Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- From Noise to Knowledge: Diffusion Probabilistic Model-Based Neural Inference of Gene Regulatory Networks.Journal of computational biology : a journal of computational molecular cell biology · 2024Article
- Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.Journal of cellular and molecular medicine · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is a chronic inflammatory disease involving cell death and inflammatory responses. Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To gain further insight, we fed ApoE-/- mice a high-fat diet to investigate the effects and mechanisms of CTSB overexpression and silencing on AS. We also explored the specific role of CTSB in vascular smooth muscle cells (VSMCs) in vitro. The study revealed that high-fat diet led to the formation of AS plaques, and CTSB was found to increase the AS plaque lesion area. Immunohistochemical and TUNEL/caspase-1 staining revealed the existence of pyroptosis in atherosclerotic plaques, particularly in VSMCs. In vitro studies, including Hoechst 33342/propidium iodide staining, a lactate dehydrogenase (LDH) release assay, detection of protein indicators of pyroptosis, and detection of interleukin-1β (IL-1β) in cell culture medium, demonstrated that oxidized low-density lipoprotein (ox-LDL) induced VSMC pyroptosis. Additionally, CTSB promoted VSMC pyroptosis. Ox-LDL increased the expression of CTSB, which in turn activated the NOD-like receptor protein 3 (NLRP3) inflammasome and promoted NLRP3 expression by facilitating nuclear factor kappa B (NF-κB) p65 nuclear translocation. This effect could be attenuated by the NF-κB inhibitor SN50. Our research found that CTSB not only promotes VSMC pyroptosis by activating the NLRP3 inflammasome, but also increases the expression of NLRP3.
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