ReviewJournal of cellular and molecular medicine2024
Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.
Review in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
The trial behind it
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
14 citing papers in PubMed.
- Preclinical evaluation of cysteine protease-inhibitor aloxistatin (E64d) for heart failure therapy.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Macrophage-derived cathepsin B disrupts intestinal tight junctions through occludin degradation and promotes alcohol-associated liver disease.Journal of hepatology · 2026Article
- Cathepsin B ablation alleviates VSMC phenotypic switching by modulating alternative macrophage polarization through the NLRP3 signaling pathway.Frontiers in cardiovascular medicine · 2026Article
- Article
- METTL3 promotes chondrocyte injury in osteoarthritis by increasing CTSB expression.Journal of orthopaedic surgery and research · 2025Article
- Cathepsin B in human peripheral blood lymphocytes as a peripheral biomarker for cardiac hypertrophy.Scientific reports · 2025Article
- Stefin A Regulation of Cathepsin B Expression and Localization in Cancerous and Non-Cancerous Cells.International journal of molecular sciences · 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
- The Emerging Roles of Vacuolar-Type ATPase-Dependent Lysosomal Acidification in Cardiovascular Disease.Biomolecules · 2025Review
- Single-cell and spatial analysis reveals the interaction between ITLN1Frontiers in cardiovascular medicine · 2025Article
- Cathepsin B induces kidney diseases through different types of programmed cell death.Frontiers in immunology · 2025Review
- RNA binding proteins potentially regulate alternative splicing of immune-related genes during the progression of coronary artery disease.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.Journal of cellular and molecular medicine · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Cathepsin B (CTSB) is a member of the cysteine protease family, primarily responsible for degrading unnecessary organelles and proteins within the acidic milieu of lysosomes to facilitate recycling. Recent research has revealed that CTSB plays a multifaceted role beyond its function as a proteolytic enzyme in lysosomes. Importantly, recent data suggest that CTSB has significant impacts on different cardiac pathological conditions, such as atherosclerosis (AS), myocardial infarction, hypertension, heart failure and cardiomyopathy. Especially in the context of AS, preclinical models and clinical sample imaging data indicate that the cathepsin activity-based probe can reliably image CTSB activity in foam cells and atherosclerotic plaques; concurrently, it allows synchronous diagnostic and therapeutic interventions. However, our knowledge of CTSB in cardiovascular disease is still in the early stage. This paper aims to provide a comprehensive review of the significance of CTSB in cardiovascular physiology and pathology, with the objective of laying a theoretical groundwork for the development of drugs targeting CTSB.
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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 Socratic graph.