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Related Concept Videos

Physiological Foundation of Stress01:24

Physiological Foundation of Stress

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Stress triggers a coordinated physiological response involving the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis. This dual activation ensures that the body is prepared for both immediate and prolonged stress management. The process begins with the perception of a stressor. This initial phase activates the SNS, leading to the rapid release of adrenaline (epinephrine) from the adrenal glands.
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Traumatic Memory01:20

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Emotionally traumatic events often lead to memories that are exceptionally vivid and enduring, sometimes persisting with remarkable clarity throughout an individual's life. A classic example of this phenomenon is a person who survives a car accident. Even years later, they may recall every detail of the event with startling accuracy — the screeching of the tires, the jarring impact, and the acrid smell of burning rubber. Such vividness contrasts sharply with how an individual...
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Updated: Apr 17, 2026

A Chronic Immobilization Stress Protocol for Inducing Depression-Like Behavior in Mice
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Cellular memory of sub-lethal stress.

Stephen W G Tait1, Andrew Oberst2

  • 1Cancer Research UK Scotland Institute, Glasgow, UK; School of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.

Immunity
|April 15, 2026
PubMed
Summary
This summary is machine-generated.

Sub-lethal activation of cell death programs, not external stresses, may drive chronic inflammation, aging, and cancer. These intrinsic pathways, when not fully triggered, can lead to long-term tissue damage and disease.

Keywords:
agingapoptosisferroptosisinflammationinnate immunitynecroptosispyroptosissenescence

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pathology

Background:

  • Regulated cell death (RCD) processes like apoptosis, pyroptosis, necroptosis, and ferroptosis are crucial for normal biological functions.
  • Proteins mediating RCD have potent activities (proteolysis, pore formation, DNA cleavage, inflammation) that can cause damage.
  • Traditionally, RCD proteins are viewed as drivers of cell death.

Purpose of the Study:

  • To explore the hypothesis that sub-lethal activation of intrinsic cell death programs is a key mediator of long-term tissue changes.
  • To investigate the implications of non-lethal RCD pathway activation in chronic inflammation, aging, and tumorigenesis.

Main Methods:

  • Conceptual review and discussion of existing literature on regulated cell death pathways.
  • Analysis of the dual role of RCD proteins in cell death versus sub-lethal pathway activation.
  • Synthesis of evidence linking sub-lethal RCD activation to disease pathology.

Main Results:

  • Sub-lethal activation of RCD pathways can promote sustained inflammation.
  • Non-lethal activation of these pathways is linked to cellular senescence.
  • Sub-lethal RCD signaling may contribute to oncogenic transformation.

Conclusions:

  • Sub-lethal activation of intrinsic cell death programs, rather than the initiating stress, may be a critical factor in chronic tissue alteration.
  • This perspective has significant implications for understanding and potentially treating chronic inflammatory diseases, aging processes, and cancer development.