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Interleukin-17A Exacerbates the Development of High-Salt-Induced Hypercholesterolemia.

Yanan Ouyang1,2,3, Jianxin Ni1, Man Wang4

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High salt intake elevates blood pressure and cholesterol by activating the IL-17 signaling pathway. Inhibiting IL-17A may treat salt-induced hypertension and hypercholesterolemia.

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comorbid mechanismdyslipidemiahigh salt diethypertensioninterleukin‐17

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Area of Science:

  • Molecular Biology
  • Cardiovascular Physiology
  • Metabolic Homeostasis

Background:

  • Dietary salt intake is a major risk factor for hypertension and cardiovascular disease.
  • The precise molecular mechanisms linking high salt consumption to dyslipidemia remain incompletely understood.
  • Interleukin-17 (IL-17) signaling has been implicated in inflammatory conditions, but its role in salt-induced metabolic dysfunction is unclear.

Purpose of the Study:

  • To elucidate the molecular pathways by which high salt diet (HSD) influences blood pressure and cholesterol metabolism.
  • To investigate the role of IL-17 signaling in mediating the adverse effects of HSD.
  • To evaluate the therapeutic potential of targeting the IL-17 pathway for salt-induced hypertension and hypercholesterolemia.

Main Methods:

  • Establishment of a hypertension and hypercholesterolemia model in Dahl salt-sensitive rats fed an 8% NaCl diet.
  • RNA sequencing (RNA-seq) and reverse transcription quantitative polymerase chain reaction (RT-qPCR) to analyze gene expression in liver tissues.
  • In vitro studies using HepG2 cells and human umbilical vein endothelial cells (HUVECs) to assess IL-17 receptor A (IL-17RA) function and its effect on sterol regulatory element-binding protein 2 (SREBP2) and nitric oxide (NO) production.
  • In vivo administration of a rat-specific anti-IL-17A antibody.

Main Results:

  • HSD successfully induced hypertension, elevated serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) in rats.
  • Cholesterol biosynthesis pathways were activated in the liver, correlating with elevated serum cholesterol.
  • IL-17 signaling activation was identified as a key factor, promoting SREBP2 nuclear entry and inhibiting NO production in endothelial cells.
  • Anti-IL-17A antibody treatment significantly reduced blood pressure and improved lipid profiles in HSD-fed rats.

Conclusions:

  • High salt diet promotes hypertension and hypercholesterolemia by activating the IL-17 signaling pathway.
  • IL-17RA signaling upregulates cholesterol biosynthesis via SREBP2 and impairs endothelial function by reducing nitric oxide production.
  • Targeting IL-17A represents a promising therapeutic strategy for managing salt-induced cardiovascular and metabolic disorders.