ArticleRenal failure2024
LPS-induced senescence of macrophages aggravates calcification and senescence of vascular smooth muscle cells via IFITM3.
Article in Renal failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting senescence-associated secretory phenotype macrophage: apigenin inhibits DOT1L-dependent H3K79me2 atFrontiers in molecular biosciences · 2026Article
- Associations between systemic inflammation response index and abdominal aortic calcification: a cross-sectional study.Scientific reports · 2025Article
- A Prominent Pro-Inflammatory Phenotype Is Observed in Replication and Stress-Induced Senescent Mast Cells.Aging cell · 2025Article
- Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease.Cell death & disease · 2025Article
- Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.Cancer biology & medicine · 2025Review
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025Review
- Comparative evaluation of cellular senescence in naturally aged and stress-induced murine macrophages for identifying optimum senescent macrophage study systems.Molecular biology reports · 2025Article
- The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.International journal of biological sciences · 2025Review
- From Bench to Bedside: Translating Cellular Rejuvenation Therapies into Clinical Applications.Cells · 2024Review
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Authors and funding
10 authors.
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Abstract
backgroundCellular senescence, macrophages infiltration, and vascular smooth muscle cells (VSMCs) osteogenic transdifferentiation participate in the pathophysiology of vascular calcification in chronic kidney disease (CKD). Senescent macrophages are involved in the regulation of inflammation in pathological diseases. In addition, senescent cells spread senescence to neighboring cells via Interferon-induced transmembrane protein3 (IFITM3). However, the role of senescent macrophages and IFITM3 in VSMCs calcification remains unexplored.
aimsTo explore the hypothesis that senescent macrophages contribute to the calcification and senescence of VSMCs via IFITM3.
methodsHere, the macrophage senescence model was established using Lipopolysaccharides (LPS). The VSMCs were subjected to supernatants from macrophages (MCFS) or LPS-induced macrophages (LPS-MCFS) in the presence or absence of calcifying media (CM). Senescence-associated β-galactosidase (SA-β-gal), Alizarin red (AR), immunofluorescent staining, and western blot were used to identify cell senescence and calcification.
resultsThe expression of IFITM3 was significantly increased in LPS-induced macrophages and the supernatants. The VSMCs transdifferentiated into osteogenic phenotype, expressing higher osteogenic differentiation markers (RUNX2) and lower VSMCs constructive makers (SM22α) when cultured with senescent macrophages supernatants. Also, senescence markers (p16 and p21) in VSMCs were significantly increased by senescent macrophages supernatants treated. However, IFITM3 knockdown inhibited this process.
conclusionsOur study showed that LPS-induced senescence of macrophages accelerated the calcification of VSMCs
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