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Updated: Apr 17, 2026

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High-Salt Diet-Induced Endothelial Dysfunction Is Mediated by Cellular Senescence.

André F Nascimento1,2, Renata A M Luvizotto1,2, Rafael M Costa1

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Journal of the American Heart Association
|April 16, 2026
PubMed
Summary
This summary is machine-generated.

High salt intake causes vascular senescence and dysfunction, but senolytic drugs can prevent these effects. Targeting inflammation, like interleukin-16 (IL16) signaling, may treat salt-sensitive vascular diseases.

Keywords:
cellular senescenceendothelial functionnavitoclaxnitric oxidevascular reactivity

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Area of Science:

  • Cardiovascular Research
  • Vascular Biology
  • Aging Research

Background:

  • High salt (HS) intake is a cardiovascular risk factor.
  • Mechanisms linking HS to endothelial dysfunction are unclear.
  • This study investigates HS-induced vascular senescence and dysfunction.

Purpose of the Study:

  • To determine if HS induces vascular senescence and dysfunction.
  • To assess if targeting senescent cells can prevent these effects.
  • To explore the role of immune activation and IL16 signaling.

Main Methods:

  • Mice were fed a high-salt diet (HSD) for 14 or 28 days.
  • Vascular function was assessed using wire myography.
  • Senescence markers (p21, p16) and inflammatory cytokines (IL-6, IL-1β, IL16) were measured.
  • Senolytic drug navitoclax was administered to test reversibility.

Main Results:

  • A 28-day HSD induced endothelial dysfunction and vascular senescence.
  • Navitoclax treatment reduced senescence markers and improved vascular function.
  • HSD increased inflammatory gene expression and circulating IL16 levels.
  • Recombinant IL16 induced endothelial dysfunction and senescence markers in vitro.

Conclusions:

  • Prolonged HSD intake causes vascular senescence and dysfunction, driven by immune activation.
  • Senolytic therapy effectively prevents HSD-induced vascular dysfunction.
  • Targeting senescence or IL16 signaling offers potential therapeutic strategies for salt-sensitive vascular diseases.