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Blocking Sigmar1 exacerbates methamphetamine-induced hypertension.

Zhen-Zhen Xu1, Jie Zhou1, Ke Duan1

  • 1Guangzhou Key Laboratory of Forensic Multi-Omics for Precision Identification, School of Forensic Medicine, Southern Medical University, Guangzhou 510515, PR China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|June 8, 2024
PubMed
Summary
This summary is machine-generated.

Chronic methamphetamine exposure causes hypertension by promoting vascular fibrosis. Sigma1 receptor (Sigmar1) plays a key role, and targeting it may offer new treatments for methamphetamine-induced hypertension.

Keywords:
HypertensionMethamphetamineSigmar1Vascular fibrosis

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Area of Science:

  • Cardiovascular Pharmacology
  • Vascular Biology
  • Drug-Induced Conditions

Background:

  • Chronic methamphetamine (METH) exposure is a significant risk factor for developing hypertension.
  • The precise mechanisms driving METH-induced hypertension and associated vascular changes are not fully understood.

Purpose of the Study:

  • To elucidate the underlying mechanisms of METH-induced hypertension.
  • To investigate the role of the Sigma1 receptor (Sigmar1) in METH-induced vascular remodeling and hypertension.

Main Methods:

  • A mouse model of METH-induced hypertension was established.
  • Vascular remodeling, blood pressure (BP), and Sigmar1 expression were assessed in METH-exposed wild-type (WT) and Sigmar1 knockout (KO) mice.
  • Mice were pretreated with a Sigmar1 antagonist (BD1047) or agonist (PRE-084) before METH exposure.
  • The differentiation of vascular smooth muscle cells (VSMCs) and mesenchymal stem cells, collagen secretion, and the TGF-β/Smad2/3 signaling pathway were analyzed.

Main Results:

  • METH exposure led to increased BP, vascular remodeling with collagen deposition, and elevated Sigmar1 levels in WT mice.
  • Sigmar1 KO mice and antagonist-treated mice exhibited exacerbated hypertension and vascular fibrosis following METH exposure.
  • Agonist treatment prevented METH-induced increases in BP and collagen.
  • METH induced VSMC and stem cell differentiation into myofibroblast-like cells, increasing collagen secretion.
  • Sigmar1 was found to suppress COL1A1 expression by inhibiting the TGF-β/Smad2/3 pathway in METH-exposed cells.

Conclusions:

  • Sigmar1 plays a critical role in METH-induced hypertension and vascular fibrosis.
  • Sigmar1 mitigates METH-induced vascular damage by inhibiting the TGF-β/Smad2/3 signaling pathway.
  • Targeting Sigmar1 presents a potential therapeutic strategy for managing METH-induced hypertension and associated vascular fibrosis.