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Abstract
The role of cellular senescence (CS) in age-related diseases (ARDs) is a quickly emerging topic in aging research. Our comprehensive data mining revealed over 250 genes tightly associated with CS. Using systems biology tools, we found that CS is closely interconnected with aging, longevity and ARDs, either by sharing common genes and regulators or by protein-protein interactions and eventually by common signaling pathways. The most enriched pathways across CS, ARDs and aging-associated conditions (oxidative stress and chronic inflammation) are growth-promoting pathways and the pathways responsible for cell-extracellular matrix interactions and stress response. Of note, the patterns of evolutionary conservation of CS and cancer genes showed a high degree of similarity, suggesting the co-evolution of these two phenomena. Moreover, cancer genes and microRNAs seem to stand at the crossroad between CS and ARDs. Our analysis also provides the basis for new predictions: the genes common to both cancer and other ARD(s) are highly likely candidates to be involved in CS and vice versa. Altogether, this study shows that there are multiple links between CS, aging, longevity and ARDs, suggesting a common molecular basis for all these conditions. Modulating CS may represent a potential pro-longevity and anti-ARDs therapeutic strategy.
Highlights
Since Hayflick’s discovery of the phenomenon of cellular senescence [1], the contribution or even relevance of this phenomenon to organismal aging has been a subject for continuous debates [2,3,4,5]
One of the first questions that arise in this context is whether cellular senescence (CS) genes share any common features with LAGs and age‐related diseases (ARDs) genes
For a more specific analysis, we further addressed the following questions: (i) Are there genes common for CS and other aging/longevity-related categories? (ii) Could genes involved in CS, ARDs and in the control of life span interact via direct protein-protein interactions (PPIs) or their common partners? (iii) Is the set of CS genes enriched in genes associated with ARDs and age-related conditions? (iv) Could the expression of these genes be under the control of common regulatory molecules, miRNAs? (v) Are there common pathways for CS, ARDs and aging-associated processes?
Summary
Since Hayflick’s discovery of the phenomenon of cellular (replicative) senescence [1], the contribution or even relevance of this phenomenon to organismal aging has been a subject for continuous debates [2,3,4,5]. The question still remains open, an increasing amount of evidence, especially from recent years, indicates that cellular senescence (CS) could have a role in aging and age-related diseases (ARDs), rather than being just a laboratory phenomenon [3, 6,7,8,9,10,11]. At least some features of CS were found in classical post-mitotic cells such as neurons, myocardiocytes and adipocytes (reviewed by Tchkonia et al [19])
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