Neutrophils: mediating TelOxidation and senescence
Maria Sol Jacome Burbano1, Julien Cherfils-Vicini1, Eric Gilson1,2
1CNRS, INSERM, IRCAN, Faculty of Medicine, Côte d'Azur University, Nice, France.
The EMBO Journal
|April 21, 2021
Summary
Neutrophils accelerate cellular senescence, a key aging factor, by transmitting reactive oxygen species (ROS). This oxidative stress primarily damages telomeres, linking oxidative stress, telomere length, and aging.
Area of Science:
- Cellular and Molecular Biology
- Immunology
- Gerontology
Background:
- Cellular senescence is a significant contributor to the aging process.
- The precise mechanisms driving the accumulation of senescent cells over time are not fully understood.
Purpose of the Study:
- To investigate the role of neutrophils in inducing cellular senescence.
- To identify the molecular mechanisms by which neutrophils might promote senescence.
Main Methods:
- The study by Lagnado et al. (2021) examined the interaction between neutrophils and neighboring cells.
- Analysis focused on the transmission of reactive oxygen species (ROS) and their effects on cellular components.
Main Results:
- Neutrophils were found to transmit reactive oxygen species (ROS) to adjacent cells, triggering senescence.
- The primary genomic targets of ROS-induced damage by neutrophils were identified as telomeres.
- This highlights a connection between telomere homeostasis and oxidative stress in senescence.
Conclusions:
- Neutrophils play a direct role in promoting cellular senescence through ROS transmission.
- Oxidative stress, particularly its impact on telomeres, is intimately linked to senescence and the aging process.
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