ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Inflammaging in periodontal, periapical, and malignancy-associated disease: drivers of alveolar bone loss and repair.Journal of bone and mineral metabolism · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
Accumulation of senescent cells in the bone microenvironment, including bone marrow mesenchymal stromal cells (BM-MSCs), contributes to aging-related bone degeneration. Developmental endothelial locus-1 (DEL-1), the expression of which declines with old age is herein described as an endogenous secreted senolytic protein. DEL-1 promotes apoptosis of senescent BM-MSCs via a β3 integrin/CD73/adenosine/p38 mitogen-activated protein kinase (p38 MAPK)/B-cell lymphoma-2 (BCL-2) pathway, thereby leading to their clearance by macrophages. DEL-1-deficiency displays increased abundance of β3 integrin-rich CD73
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Registered trials
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