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Induction and Validation of Cellular Senescence in Primary Human Cells
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A BDNF-TrkB autocrine loop enhances senescent cell viability.

Carlos Anerillas1, Allison B Herman2, Rachel Munk2

  • 1Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, MD, USA. carlos.anerillasaljama@nih.gov.

Nature Communications
|October 20, 2022
PubMed
Summary
This summary is machine-generated.

Targeting TrkB (NTRK2) inhibitors selectively induces apoptosis in senescent cells. This approach reduces the senescent cell burden in aged mice by blocking the autocrine BDNF-TrkB survival pathway.

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Area of Science:

  • Cellular biology
  • Aging research
  • Molecular medicine

Background:

  • Cellular senescence, marked by cell cycle arrest and a senescence-associated secretory phenotype (SASP), contributes to age-related diseases.
  • Current aging interventions focus on eliminating senescent cells to mitigate SASP-driven pathologies.

Purpose of the Study:

  • To identify therapeutic targets for selectively eliminating senescent cells.
  • To investigate the role of TrkB signaling in senescent cell survival.

Main Methods:

  • Drug library screening to identify TrkB inhibitors.
  • Assessing the effect of TrkB inhibition on senescent and proliferating human cells.
  • Investigating the BDNF-TrkB-ERK5-BCL2L2 pathway in senescent cells.
  • Evaluating TrkB inhibitor efficacy in aged mouse models.

Main Results:

  • TrkB inhibitors induced apoptosis in senescent cells but not proliferating cells.
  • Senescent cells exhibited high TrkB expression and secreted BDNF, activating an autocrine loop.
  • This loop involved ERK5 activation and elevated BCL2L2, promoting survival.
  • TrkB inhibition reduced senescent cell accumulation in aged mouse organs.

Conclusions:

  • TrkB signaling, activated by the SASP factor BDNF, is crucial for senescent cell survival.
  • TrkB inhibitors represent a potential therapeutic strategy to reduce the senescent cell burden in aging.
  • Targeting the BDNF-TrkB pathway offers a novel approach for aging interventions.