Cellular senescence and the senescent secretory phenotype: therapeutic opportunities.

By T. Tchkonia, Yi Zhu, J. V. van Deursen, J. Campisi, J. Kirkland. Journal of Clinical Investigation, 2013

1,571 citations recorded by the source corpus.

Subfields: Aging, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/d7dea011e091219a471af01899530c451974f460

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. J. Kirkland
2. T. Tchkonia
3. Jesús Gil
4. Luigi Ferrucci
5. J. Campisi
6. Y. Fouad
7. C. Aanei

In Immunology

1. J. Kirkland
2. T. Tchkonia
3. Jesús Gil
4. J. Campisi
5. Claudio Franceschi
6. Yi Zhu
7. Luigi Ferrucci
8. Y. Fouad

In Physiology

1. J. Kirkland
2. T. Tchkonia
3. Jesús Gil
4. J. Campisi
5. Nicolás Herranz
6. Nathan K. LeBrasseur
7. Claudio Franceschi
8. Yi Zhu

Citations in the corpus

• A proteomic atlas of senescence-associated secretomes for aging biomarker development (2019, background): “The SASP consists of a 42 myriad of cytokines, chemokines, growth factors and proteases that initiate 43 inflammation, wound healing and growth responses in nearby cells [5,6].”
• Cellular Senescence: A Translational Perspective (2017, background): “(Tchkonia et al., 2013; LeBrasseur et al., 2015).”
• The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates (2018, background): “One of the most advanced and appealing hypotheses is that environmental stressors may contribute to age-related neurodegeneration by favoring cell senescence of glia, thus creating a chronically inflamed milieu in the brain (167).”
• Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence (2017, neutral): “A prominent hallmark of senescent cells is the secretion of inflammatory mediators, including various cytokines, chemokines, extracellular matrix proteins and growth factors, collectively referred to as the senescence-associated secretory phenotype (SASP)3 4.”
• Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “A number of additional tissues undergo senescence with age and disease (reviewed in [14,128, 140, 141]); however, additional studies are needed to understand the contribution of these senescent cells to disease initiation, progression, and maintenance.”
• mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype (2015, positive): “As rapamycin extends the lifespan of mice 21 , and the ablation of senescent cells improves age-related diseases 26,27 , downregulating the SASP could contribute to the benefits observed in rapamycin-treated old mice.”
• Ionizing radiation reduces ADAM10 expression in brain microvascular endothelial cells undergoing stress-induced senescence (2017, background): “In addition, identification of unique surface markers may potentially allow development of novel therapeutic approaches to target removal or attenuation of inflammatory senescent cells through vascular targeting [25-27].”
• The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (2015, background): “examined in animalmodels of other conditionsor diseases towhich cellular senescence may contribute to pathogenesis, including diabetes, neurodegenerative disorders, osteoarthritis, chronic pulmonary disease, renal diseases, and others (Tchkonia et al., 2013; Kirkland & Tchkonia, 2014).”