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The dissolution of intimate relationships presents complex emotional and psychological challenges, particularly when emotional bonds are strong, the relationship is long-standing, and perceived alternatives are limited. This distress often intensifies in romantic breakups, where the initiator may experience greater turmoil than the rejected partner. Contributing factors include residual attachment, guilt over causing pain, and uncertainty about how to manage the situation. The stress is further...
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Updated: Jan 23, 2026

Far-Red Fluorescent Senescence-Associated β-Galactosidase Probe for Identification and Enrichment of Senescent Tumor Cells by Flow Cytometry
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Mitochondrial dysfunction and cell senescence: deciphering a complex relationship.

James Chapman1, Edward Fielder1, João F Passos1,2

  • 1Institute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, UK.

FEBS Letters
|June 19, 2019
PubMed
Summary
This summary is machine-generated.

Cellular senescence and mitochondrial dysfunction are key to aging. This review explores their link, focusing on how mitochondria influence the inflammatory SASP and potential therapeutic targets.

Keywords:
ageingmitochondriasenescencesenolyticssenostatics

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Area of Science:

  • Gerontology
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Cellular senescence and mitochondrial dysfunction are recognized hallmarks of aging.
  • Cellular senescence drives aging and age-related diseases.
  • Mitochondria are increasingly understood as key regulators of senescence.

Purpose of the Study:

  • To review the relationship between cellular senescence and mitochondrial dysfunction.
  • To highlight the role of mitochondria in the senescence-associated secretory phenotype (SASP).
  • To explore therapeutic strategies targeting mitochondrial-senescence interactions.

Main Methods:

  • Literature review of cellular senescence and mitochondrial biology.
  • Analysis of homeostatic mechanisms, reactive oxygen species, and metabolites in senescence.
  • Discussion of mitochondrial-mediated pathways influencing SASP.

Main Results:

  • Mitochondria significantly modulate the senescence phenotype.
  • Mitochondrial dysfunction contributes to the pro-inflammatory SASP.
  • Homeostatic mechanisms, ROS, and metabolites are involved in senescence.

Conclusions:

  • The interplay between mitochondria and senescence is critical in aging.
  • Understanding mitochondrial roles in SASP offers therapeutic potential.
  • Targeting these pathways may lead to novel anti-aging interventions.