ArticleMolecular medicine reports2020
Cathepsin B aggravated doxorubicin‑induced myocardial injury via NF‑κB signalling.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Cathepsin B ablation alleviates VSMC phenotypic switching by modulating alternative macrophage polarization through the NLRP3 signaling pathway.Frontiers in cardiovascular medicine · 2026Article
- Metalloimmunotherapies: metal-driven regulatory networks in the immune microenvironment.Frontiers in immunology · 2026Review
- Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.Frontiers in pharmacology · 2026Article
- Cathepsin B-dependent glycolysis contributes to reduced renal uric acid excretion in hyperuricemia.Communications biology · 2025Article
- GLP1 alleviates oleic acid-propelled lipocalin-2 generation by tumor-infiltrating CD8Cellular & molecular immunology · 2025Article
- Cathepsin Levels and Atrial Fibrillation Risk: Insights From Bidirectional and Multivariable Mendelian Randomization Analyses.International journal of genomics · 2025Article
- Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.Journal of cellular and molecular medicine · 2024Review
- Article
- PGC-1α Agonist Rescues Doxorubicin-Induced Cardiomyopathy by Mitigating the Oxidative Stress and Necroptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Gene Networks of Hyperglycemia, Diabetic Complications, and Human Proteins Targeted by SARS-CoV-2: What Is the Molecular Basis for Comorbidity?International journal of molecular sciences · 2022Article
- Histone deacetylase 3 facilitates TNFα-mediated NF-κB activation through suppressing CTSB induced RIP1 degradation and is required for host defense against bacterial infection.Cell & bioscience · 2022Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocyte apoptosis and oxidative stress key critical roles in the process of doxorubicin (DOX)‑induced cardiotoxicity. However, how apoptosis and oxidative stress arise in DOX‑induced heart injury remains largely unknown. Cathepsin B (CTSB) is a typical lysosomal cysteine protease that is associated with apoptosis, inflammatory responses, oxidative stress and autophagy. The present study aimed to investigate the role of CTSB in DOX‑induced heart injury and its potential mechanism. H9C2 cells were infected with adenovirus or transfected with small interfering RNA to overexpress or knock down CTSB, respectively, and then stimulated with DOX. DOX induced increased CTSB expression levels in H9C2 cells. DOX‑induced cardiomyocyte apoptosis and oxidative stress were attenuated by CTSB knockdown but aggravated by CTSB overexpression in vitro. Mechanistically, the present study showed that CTSB activated the NF‑κB pathway in response to DOX. In summary, CTSB aggravated DOX‑induced H9C2 cell apoptosis and oxidative stress via NF‑κB signalling. CTSB constitutes a potential therapeutic target for the treatment of DOX‑induced cardiotoxicity.
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