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Updated: May 30, 2025

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Targeting CRM1 for Progeria Syndrome Therapy.

Adriana Soto-Ponce1, Marlon De Ita1,2, Susana Castro-Obregón3

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Summary
This summary is machine-generated.

Selinexor, a CRM1 inhibitor, shows promise in treating Hutchinson-Gilford progeria syndrome (HGPS) by reducing progerin levels and mitigating cellular senescence. This drug offers a potential therapeutic strategy for HGPS and other aging disorders.

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agingprogeriasenescence

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Area of Science:

  • Cell Biology
  • Genetics
  • Pharmacology

Background:

  • Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by progerin, a mutant lamin A variant, leading to nuclear envelope abnormalities and cellular senescence.
  • Overexpression of chromosomal region maintenance 1 (CRM1) enhances nuclear export in HGPS fibroblasts, and its inhibition with leptomycin B rescues senescence.
  • CRM1 is identified as a potential therapeutic target for HGPS.

Purpose of the Study:

  • To investigate the therapeutic potential of selinexor, a selective CRM1 inhibitor, in HGPS.
  • To evaluate the effects of selinexor on progerin clearance, cellular senescence, and gene expression in HGPS patient-derived cells.
  • To assess the in vivo efficacy of selinexor in a mouse model of progeria.

Main Methods:

  • Treatment of HGPS patient-derived dermal fibroblasts and LMNAG609G/G609G mice with selinexor.
  • Analysis of cellular senescence, progerin levels (immunostaining, immunoblotting), gene expression, and aortic histopathology.
  • Pharmacological modulation of CRM1 activity.

Main Results:

  • Selinexor treatment mitigated senescence and promoted progerin clearance via autophagy in HGPS fibroblasts.
  • Transcriptional analysis revealed restoration of numerous differentially-expressed genes and rescued aging-associated cellular processes.
  • In vivo, selinexor decreased progerin levels and improved aortic histopathology in progeric mice.

Conclusions:

  • Selinexor demonstrates geroprotective effects in HGPS by normalizing nucleocytoplasmic protein distribution and reducing progerin levels.
  • Selinexor acts through at least two mechanisms: modulating the aging-associated transcriptome and decreasing progerin.
  • Further research into selinexor's effects on cardiovascular function in progeric mice is warranted for HGPS and aging disorder therapeutics.