Targeting cellular senescence to combat cancer and ageing

Wang, Chen; Hou, Xue; Zhang, Rugang

doi:10.1002/1878-0261.13266

Cited by 10 publications

(6 citation statements)

References 173 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings may indicate some association between smoking and aging. Cellular senescence includes inflammation, fibrosis, metabolic disorders, DNA damage, mitochondrial dysfunction, loss of protein homeostasis, failed autophagy, Reactive Oxygen Species generation, NAD + depletion, and stem/progenitor cell dysfunction [31][32][33] . A mixture of thousands of chemicals is created by burning or heating tobacco when people smoke.…”

Section: Discussionmentioning

confidence: 99%

Association between cigarette smoking and serum alpha klotho levels among US adults over 40-years-old: a cross-sectional study

Du,

Tang,

Jiang

et al. 2023

Sci Rep

View full text Add to dashboard Cite

Alpha klotho (α-Klotho) is an anti-aging molecule associated with aging and several diseases. Previous studies have reported inconsistent levels of α-Klotho in smokers. This study aimed to demonstrate serum α-Klotho levels in smokers among the US population. This cross-sectional study recruited 11,559 participants (aged 40–79 years; 48.2% males). All data were collected from the 2007–2016 National Health and Nutrition Examination Survey. The study comprised adults with reliable Klotho and smoking questionnaire results. The relationship between smoking and serum α-klotho levels was assessed using multivariate linear regression models after adjusting for potential confounders. We also performed a stratified analysis of clinically important variables. The mean serum α-klotho level among the 11,559 participants was 843.85 pg/mL. After full adjustment, habitual smoking was significantly associated with decreased serum levels of α-klotho level (β = − 34.89; 95% CI − 54.97, − 14.81; P = 0.0013) in the total study population. Furthermore, the stratified analysis indicated that the association was insignificant in the 60–79 age group. Quitting smoking was not significantly associated with serum levels of α-klotho as expected (P = 0.1148) in the total study population. However, stratified analyses showed a significant inversed association in the male, those with chronic kidney disease, or those with cancer who quit smoking (all P < 0.05). Cigarette smoking was inversely associated with serum α-Klotho levels among US adults.

show abstract

Section: Discussionmentioning

confidence: 99%

Association between cigarette smoking and serum alpha klotho levels among US adults over 40-years-old: a cross-sectional study

Du,

Tang,

Jiang

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Telomere attrition to a critical threshold length that is no longer able to sustain telomere integrity is one of several known inducers of cellular senescence [50]. This type of senescence, termed telomere-induced or replicative senescence, can be triggered by the well-known tumour suppressor p53 and its downstream effector p21, a cyclin-dependent kinase inhibitor that represses the cell cycle (as discussed in an accompanying article in this special series [51,52]). Mathematical models and studies of budding yeast have suggested that the shortest telomeres are responsible for senescence induction [53,54].…”

Section: Telomere Erosion: a Harbinger Of Senescencementioning

confidence: 99%

“…Senescent cells secret specific small molecules or exosomes (EV) that interact with and influence the nearby environment. This phenomenon is known more generally as the Senescence-Associated Secretory Phenotype (SASP) and is a phenotype common to many senescent states, including that induced by eroded telomeres (please see accompanying review) [51,52,62,65,66] (Fig. 2).…”

Section: Telomere Erosion: a Harbinger Of Senescencementioning

confidence: 99%

Tieing together loose ends: telomere instability in cancer and aging

2022

View full text Add to dashboard Cite

Telomere maintenance is essential for maintaining genome integrity in both normal and cancer cells. Without functional telomeres, chromosomes lose their protective structure and undergo fusion and breakage events that drive further genome instability, including cell arrest or death. One means by which this loss can be overcome in stem cells and cancer cells is via re‐addition of G‐rich telomeric repeats by the telomerase reverse transcriptase (TERT). During aging of somatic tissues, however, insufficient telomerase expression leads to a proliferative arrest called replicative senescence, which is triggered when telomeres reach a critically short threshold that induces a DNA damage response. Cancer cells express telomerase but do not entirely escape telomere instability as they often possess short telomeres; hence there is often selection for genetic alterations in the TERT promoter that result in increased telomerase expression. In this review, we discuss our current understanding of the consequences of telomere instability in cancer and aging, and outline the opportunities and challenges that lie ahead in exploiting the reliance of cells on telomere maintenance for preserving genome stability.

show abstract

“…Senescence-associated proliferation arrest and SASP cooperate in tumor suppression, by arresting proliferation of damaged pre-malignant cells and promoting immune clearance. Although senescence is acutely tumor suppressive, over the longer term, as a source of chronic inflammation, SASP also promotes tissue aging and disease, as reviewed by Rugang Zhang and colleagues [52] and Naoko Ohtani and colleagues [53].…”

Section: Other Potential Causes Of Age-associated Cancermentioning

confidence: 99%