Cellular senescence: a key process in cell cycle regulation

Cellular senescence refers to a permanent state of cell cycle arrest triggered by stress, including replicative senescence (RS) and stress-induced premature senescence (SIPS). This process occurs in response to DNA damage, telomere shortening, oncogenic mutations, and other cellular stressors.

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Pathways to cellular senescence in eukaryotic cells. Multiple discrete cellular insults act via distinct signaling mechanisms to induce cell-cycle arrest in the kidney at either the G1/S (via inhibition of cdk2 and/or cdk4/6) or G2/M checkpoints (via Chk1/2 activation or cdc2/25c inhibition). Inactivation of oncogenes and spindle/epigenetic/nucleolar stress trigger activation of the cyclin-dependent kinase inhibitor p16ink4a. Telomere shortening, DNA damage, mitogen or oncogene activation, and hypoxia/reoxygenation also result in G1/S cell-cycle arrest, via a pathway dependent on p53 and p21cip1 activation. In contrast to this, developmental senescence appears to induce p21cip1 by pathways mediated by TGFb/PI3K and independent of p53. ATM/ATR/ARF, Ataxia–Telangiectasia Mutated/Ataxia Telangiectasia and Rad3-related protein/p14 Alternate Reading Frame (human).

What causes cellular senescence ?

Senescence in cells can be induced by various stressors:

DNA Damage: Caused by critical telomere shortening, injury, or exposure to genotoxic agents.
Oncogenic Stress: Activation of oncogenes that trigger cell cycle arrest.
Metabolic Dysregulation: Mitochondrial dysfunction or protein misfolding.
Inflammatory Signals: Cytokines and chemokines that influence the senescence pathway.
Aging and Disease: Chronic stress associated with aging and degenerative disorders.

The senescence program is closely linked to the inhibition of the cell cycle machinery, with its phenotype varying based on the stress signals, cell type, and environment.

Senescent cells and their unique characteristics

Senescent cells exhibit distinct features, including prolonged cell cycle arrest, transcriptional changes, and the secretion of bioactive molecules, collectively known as the senescence-associated secretory phenotype (SASP). These cells also experience macromolecular damage and metabolic deregulation.

Senescence acts as a protective mechanism, preventing further cellular damage by inhibiting re-entry into the cell cycle in response to mitogenic stimuli. The senescent state is marked by resistance to cell death and an enhanced secretory phenotype, helping to safeguard the organism from harmful cellular activities.

Cellular senescence and diseases

While senescence in cells acts as a barrier against tumorigenesis and plays roles in embryogenesis and tissue repair, it also contributes to pathological processes, including:

Aging-Related Disorders: Alzheimer’s disease, diabetes, and cardiovascular disease.
Kidney and Liver Diseases: Fatty liver disease and chronic kidney disease.
Cancer Progression: Though initially protective, accumulated senescent cells can promote inflammation and tumor growth over time.

Understanding senescence in cells is crucial for studying its dual roles in health and disease, making it a vital area of research.

The role of cellular senescence in tissue homeostasis and repair

Senescence in cells is not only a defensive mechanism against cancer but also plays an essential role in tissue homeostasis and repair. During wound healing and tissue regeneration, senescent cells contribute to the remodeling of tissues by secreting factors that promote inflammation and recruit immune cells. While this secretory activity helps to repair damaged tissues, an accumulation of senescent cells over time can lead to chronic inflammation, tissue dysfunction, and the progression of age-related diseases. Thus, a balanced regulation of senescence is critical for maintaining healthy tissue function throughout an organism’s life.

Potential causes and consequences of cell senescence. Several factors have been identified to induce cell senescence, including telomere shortening, oncogene activation, DNA damage,and oxidative stress. Senescent cells, on the other hand,exhibit multiple characteristics, including growth arrest, metabolic changes, altered apoptosis sensitivity, and senescence-associated secretary phenotype (SASP).

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Cellular senescence signaling pathway biomarker list

You can check the biomarker list included in this pathway, see below:

Species : Homo sapiens (human)

Human signaling pathways

Signaling Pathways	Product ref	Informations
Cellular Senescence	CS1H1	Download biomarker list

Species : Mus musculus (mouse)

Mouse signaling pathways

Signaling Pathways	Product ref	Informations
Cellular Senescence	CS1M1	Download biomarker list

Species : Rattus norvegicus (rat)

Rat signaling pathways

Signaling Pathways	Product ref	Informations
Cellular Senescence	*******	Biomarker list in progress.

Species : Sus Scrofa (Pig)

Pig signaling pathways

Signaling Pathways	Product ref	Informations
Cellular Senescence	*******	Biomarker list in progress.

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Bibliography

1. Calcinotto A, et al. Cellular Senescence: Aging, Cancer, and Injury. Physiol Rev. (2019);99(2):1047-1078.

2. Docherty MH, et al. Cellular Senescence in the Kidney. J Am Soc Nephrol. (2019);30(5):726-736.

3. Liu RM. Aging, Cellular Senescence, and Alzheimer's Disease. Int J Mol Sci. (2022);23(4):1989.

4. Roger L, Tomas F, Gire V. Mechanisms and Regulation of Cellular Senescence. Int J Mol Sci. (2021);22(23):13173.

5. Palmer AK, et al. Cellular senescence: at the nexus between ageing and diabetes. Diabetologia. (2019) ;62(10):1835-1841.

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