ArticleCommunications biology2025
Endothelial senescence drives intrinsic skin aging via the neuroimmune CGRP-mast cell axis in mice.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting the neuro-immune-skin axis: Advanced functional biomaterials for intelligent wound management and regeneration.Materials today. Bio · 2026Review
- Advances in skin aging: integrating epigenetic, cellular, and immune mechanisms for targeted therapy.Immunity & ageing : I & A · 2026Review
- Dual Roles and Therapeutic Prospects of Proximal Tubular Epithelial Cell Senescence in Acute Kidney Injury.Biomolecules · 2026Review
- Cellular senescence in migraine - a hypothesis-driven narrative review.The journal of headache and pain · 2026Review
- Bioconverted Blueberry Extract Potentiates the Angiogenic and Endothelial Functions in Human Dermal Microvascular Endothelial Cells Under Oxidative Stress.Current issues in molecular biology · 2026Article
- Vascular endothelial cells as signaling niches for epithelial stem cells in the skin.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Aging is accompanied by progressive vascular dysfunction, but its effects on skin aging remain poorly understood. Although endothelial cell (EC) senescence is implicated in various age-related diseases, its specific role in dermal aging remains unclear. Here we show that EC senescence contributes to intrinsic skin aging through immune dysregulation. Using an EC-specific senescent mouse model, we observe mast cell activation driven by the neuropeptide calcitonin gene-related peptide (CGRP), independent of traditional IgE-mediated pathways. Senescent ECs secreted pro-inflammatory senescence-associated secretory phenotype (SASP) factors, activating dermal neurons to produce CGRP, leading to mast cell degranulation and subsequent skin aging phenotypes. Pharmacological stabilization of mast cells or inhibition of the EC-SASP-CGRP pathway significantly attenuate dermal thinning, collagen degradation, and delayed wound healing, which are hallmarks of intrinsic skin aging. These findings identify vascular senescence as an upstream regulator of skin aging through a neuroimmune mechanism and suggest potential therapeutic targets for age-related skin deterioration.
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Registered trials
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