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Updated: Apr 1, 2026

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Intercompartmental communication in senescence.

Krystyna Mazan-Mamczarz1, Eleanor J Wind1, Jixiang Leng1

  • 1Laboratory of Genetics and Genomics, National Institute on Aging (NIA) Intramural Research Program (IRP), National Institutes of Health (NIH), Baltimore, MD, USA.

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|March 30, 2026
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Summary
This summary is machine-generated.

Cellular senescence, marked by growth arrest and inflammation, involves widespread organelle changes that disrupt cell communication. This breakdown in interorganelle crosstalk drives aging and disease, offering new therapeutic targets.

Keywords:
GolgiSASPendoplasmic reticuluminterorganellar communicationorganellessenescence

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Area of Science:

  • Cellular Biology
  • Aging Research
  • Molecular Medicine

Background:

  • Cellular senescence is a state of irreversible growth arrest triggered by damage.
  • Senescent cells accumulate with age, contributing to tissue dysfunction and age-related diseases.
  • These cells exhibit a pro-inflammatory senescence-associated secretory phenotype (SASP).

Purpose of the Study:

  • To review how cellular senescence alters intracellular communication networks.
  • To examine the impact of senescence on vesicular trafficking and interorganelle contact sites.
  • To highlight emerging technologies and therapeutic vulnerabilities related to senescent organelle dysfunction.

Main Methods:

  • Review of existing literature on cellular senescence and organelle remodeling.
  • Analysis of how changes in vesicular trafficking (secretory, endocytic, autophagic) affect cellular function.
  • Examination of altered interorganelle contacts (e.g., mitochondria-ER-lysosomes) and their role in signaling.

Main Results:

  • Senescence involves broad remodeling of cellular compartments, impacting homeostasis.
  • Disrupted interorganelle communication exacerbates oxidative stress, proteostatic imbalance, and impaired clearance.
  • Impaired crosstalk activates key signaling pathways (p53/p21, p16/Rb, cGAS-STING, NF-κB, mTOR), promoting apoptosis resistance and SASP.

Conclusions:

  • Cellular senescence results from both gene expression changes and disrupted interorganelle communication.
  • Senescence can be redefined as a failure of the organellar interactome.
  • Understanding these defects offers new therapeutic strategies for age-associated diseases.