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Matrix stiffness induces endothelial network senescence.

Jiyeon Song1, Alexandra N Rindone2, Ya Guan1

  • 1Department of Biomedical Engineering, Duke University, Durham, NC 27708, USA.

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|November 24, 2025
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Summary
This summary is machine-generated.

Tissue stiffening drives cellular senescence in endothelial cells, impacting aging and disease. Targeting the Notch signaling pathway offers a potential intervention for mechanoaging.

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Area of Science:

  • Cellular senescence
  • Mechanobiology
  • Vascular aging

Background:

  • Cellular senescence contributes to age-related tissue dysfunction.
  • Understanding senescence drivers is key for developing restorative interventions.
  • The role of mechanical stress in endothelial cell senescence is not fully understood.

Purpose of the Study:

  • To investigate how extracellular matrix (ECM) stiffening influences endothelial cell (EC) senescence.
  • To establish a model system to study senescence in response to mechanical stress alone.
  • To identify the molecular pathways involved in mechano-induced EC senescence.

Main Methods:

  • Developed a 3D human in vitro model to isolate mechanical stress effects.
  • Assessed EC senescence markers (p16/p21) and senescence-associated secretory phenotype (SASP).
  • Analyzed the Notch-JNK-FOS signaling axis and used pharmacologic Notch inhibition.
  • Examined fibrotic capsule tissue from patients with synthetic breast implants.
  • Utilized single-cell RNA sequencing (scRNA-seq) on patient-derived tissues.

Main Results:

  • Matrix stiffening induced an EC senescence phenotype, including elevated p16/p21 and SASP, without inflammatory signals.
  • A Notch-JNK-FOS signaling axis mediated mechano-induced senescence.
  • Notch inhibition attenuated stiffness-induced senescence.
  • Patient fibrotic tissues showed increased p16+Notch1+ endothelial cells, enriched in Notch/JNK and SASP gene programs.
  • Confirmed tissue stiffening as an upstream aging signal driving vascular senescence.

Conclusions:

  • Vascular senescence is a mechanosensitive process driven by tissue stiffening.
  • Identified a novel Notch-JNK-FOS signaling pathway in mechano-induced EC senescence.
  • The study provides a human-relevant platform for investigating endothelial mechanoaging and potential therapeutic targets.