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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
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Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Unrenewable Cells00:50

Unrenewable Cells

In humans, the photoreceptor cells of the eye and sensory hair cells of the ear lack stem cells. These cells are thus unrenewable and cannot be replaced when they are damaged or destroyed.
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The retina is composed of several layers and contains specialized cells called photoreceptors. The photoreceptors (rods and cones) change their membrane potential when stimulated by light energy. There are two types of photoreceptors—rods and cones—which differ in the shape of their outer...

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Techniques to Induce and Quantify Cellular Senescence
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Cellular Senescence in the Absence of Galactic Cosmic-Ray Muons.

Àngela Llop-Hernández1,2, Júlia López1,2, Sara Verdura1,2

  • 1Program Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology, 17007 Girona, Spain.

Aging and Disease
|June 3, 2026
PubMed
Summary

Cosmic muons, a form of cosmic background radiation (CBR), may help cells decide to enter senescence, a state of irreversible cell cycle arrest. Reduced muons specifically impacted G0/G1 arrest, suggesting a role in cellular damage response.

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Area of Science:

  • Cellular Biology
  • Astrobiology
  • Radiation Biology

Background:

  • Cellular senescence is a critical stress response preventing proliferation of damaged cells.
  • Senescence evolved in Earth's biosphere, exposed to continuous cosmic background radiation (CBR).
  • Cosmic muons, a component of CBR, are highly penetrating particles.

Purpose of the Study:

  • To investigate if cosmic muons contribute to the thresholding of cellular senescence.
  • To explore the role of abiotic stress from muons in senescence induction dynamics.

Main Methods:

  • Comparison of human cancer cell senescence induction under normal CBR and muon-depleted conditions (deep underground lab).
  • Exposure to G0/G1-targeting (palbociclib) and G2/M-targeting (alisertib, bleomycin) chemotherapeutics.
  • Assessment of senescence-associated β-gal phenotype, SENCAN classifier, secretory phenotype, and transcriptome-wide variations.

Main Results:

  • Muon depletion significantly reduced senescence-associated β-gal phenotype acquisition specifically for G0/G1 arrest induced by palbociclib.
  • Senescence states induced by G2/M arrest (alisertib, bleomycin) were unaffected by muon suppression.
  • Transcriptome-wide analysis showed minor variations in senescence pathways due to muon absence, while SENCAN and secretory profiles remained largely unchanged.

Conclusions:

  • Cosmic muons may act as abiotic signal calibrators, specifically aiding G0/G1 withdrawal senescence trajectories.
  • This suggests life evolved to utilize CBR for sensing and responding to cellular damage.
  • Findings may inform understanding of senescence in extraterrestrial environments with low muon flux.