ArticleInternational journal of molecular sciences2023
Cathepsin S Knockdown Suppresses Endothelial Inflammation, Angiogenesis, and Complement Protein Activity under Hyperglycemic Conditions In Vitro by Inhibiting NF-κB Signaling.
Article in International journal of molecular sciences, 2023. 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, 22 citations in OpenAlex.
- Hyperglycemia-Induced Microglial CTSS Disrupts Blood-Retinal Barrier Integrity via PAR2-Dependent Downregulation of Endothelial MFSD2A.CNS neuroscience & therapeutics · 2026Article
- Levels and Effects of Nogo-B in Patients With Type 2 Diabetes or Hyperglycemic HUVEC Model.Endocrinology, diabetes & metabolism · 2026Article
- Cathepsin H drives hypoxia-associated inflammatory and angiogenic programs in diabetic retinopathy and represents a potential therapeutic target.International journal of biological sciences · 2026Article
- Obesity and cathepsin S in periodontal health and disease: A prospective clinical observational study.Acta odontologica Scandinavica · 2025Observational
- Identification of Cathepsin H and Metabolic Traits as Potential Biomarkers for Lung Cancer by Mendelian Randomization and Single-Cell Transcriptomics.Advanced genetics (Hoboken, N.J.) · 2025Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- A Second Opportunity for the Peptide-Based Analogues with γ-Lactam at the P1 Position: Human Cathepsin S Inhibition.Pharmaceuticals (Basel, Switzerland) · 2025Article
- LINC02099 Promotes Retinal Extracellular Matrix Deposition in Diabetic Mice Via the miRNA-214-3p/CTSS Axis.Investigative ophthalmology & visual science · 2025Article
- Sodium-glucose cotransporter 2 inhibitors alleviate renal fibrosis in diabetic kidney disease by inhibiting Hmgcs2 and Btg2 in proximal tubular cells.Journal of translational medicine · 2025Article
- FHL2 expression by cancer-associated fibroblasts promotes metastasis and angiogenesis in lung adenocarcinoma.International journal of cancer · 2025Article
- Cathepsin S: molecular mechanisms in inflammatory and immunological processes.Frontiers in immunology · 2025Review
- Article
- Comparative study on the predictive value of TyG, TyG-BMI, and TG/HDL-C for progression-free survival in patients with locally advanced nasopharyngeal carcinoma.Frontiers in nutrition · 2025Article
- Assessment of the diagnostic value of serum cathepsin S and its correlation with HDL subclasses in patients with non-Hodgkin's lymphoma.Journal of medical biochemistry · 2024Article
- PANoptosis: Novel insight into regulated cell death and its potential role in cardiovascular diseases (Review).International journal of molecular medicine · 2024Review
- Deciphering the impact of aging on splenic endothelial cell heterogeneity and immunosenescence through single-cell RNA sequencing analysis.Immunity & ageing : I & A · 2024Article
- Cathepsin S (CTSS) in IgA nephropathy: an exploratory study on its role as a potential diagnostic biomarker and therapeutic target.Frontiers in immunology · 2024Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Hyperglycemia plays a key role in the development of microvascular complications, endothelial dysfunction (ED), and inflammation. It has been demonstrated that cathepsin S (CTSS) is activated in hyperglycemia and is involved in inducing the release of inflammatory cytokines. We hypothesized that blocking CTSS might alleviate the inflammatory responses and reduce the microvascular complications and angiogenesis in hyperglycemic conditions. In this study, we treated human umbilical vein endothelial cells (HUVECs) with high glucose (HG; 30 mM) to induce hyperglycemia and measured the expression of inflammatory cytokines. When treated with glucose, hyperosmolarity could be linked to cathepsin S expression; however, many have mentioned the high expression of CTSS. Thus, we made an effort to concentrate on the immunomodulatory role of the CTSS knockdown in high glucose conditions. We validated that the HG treatment upregulated the expression of inflammatory cytokines and CTSS in HUVEC. Further, siRNA treatment significantly downregulated CTSS expression along with inflammatory marker levels by inhibiting the nuclear factor-kappa B (NF-κB) mediated signaling pathway. In addition, CTSS silencing led to the decreased expression of vascular endothelial markers and downregulated angiogenic activity in HUVECs, which was confirmed by a tube formation experiment. Concurrently, siRNA treatment reduced the activation of complement proteins C3a and C5a in HUVECs under hyperglycemic conditions. These findings show that CTSS silencing significantly reduces hyperglycemia-induced vascular inflammation. Hence, CTSS may be a novel target for preventing diabetes-induced microvascular complications.
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