CoChat
Sign Up
Cited by 279

The DOI matches its Crossref record; 68 of the 68 references it cites were found in a registry or an index.

Cellular senescence in development, regeneration and disease

Rhinn, Muriel, Ritschka, Birgit, Keyes, William M.·2019·Development
DOI 10.1242/dev.151837
Open this paper in CoChat — free account

Abstract

Cellular senescence is a state comprising an essentially irreversible proliferative arrest combined with phenotypic changes and pronounced secretory activity. Although senescence has long been linked with aging, recent studies have uncovered functional roles for senescence in embryonic development, regeneration and reprogramming, and have helped to advance our understanding of this process as a highly coordinated and programmed cellular state. In this Primer article, we summarize some of the key findings in the field and attempt to explain them in a simple model that reconciles the normal and pathological roles for senescence. We discuss how a primary role of cellular senescence is to contribute to normal development, cell plasticity and tissue repair, as a dynamic and tightly regulated cellular program. However, when this process is perturbed, the beneficial effects turn detrimental and can contribute to disease and aging.

Overview

Integrity signals

Registry

Crossref · 10.1242/dev.151837

Cites

68 of 68 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 68 references

Research works printed but not linked: 55

  1. Achuthan, 2011, Drug-induced senescence generates chemoresistant stemlike cells with low reactive oxygen species, J. Biol. Chem., 286, 37813, 10.1074/jbc.M110.200675 · DOI
  2. Althubiti, 2014, Characterization of novel markers of senescence and their prognostic potential in cancer, Cell Death Dis., 5, e1528, 10.1038/cddis.2014.489 · DOI · Paper page
  3. Benhamed, 2012, Senescence is an endogenous trigger for microRNA-directed transcriptional gene silencing in human cells, Nat. Cell Biol., 14, 266, 10.1038/ncb2443 · DOI · Paper page
  4. Capell, 2016, MLL1 is essential for the senescence-associated secretory phenotype, Genes Dev., 30, 321, 10.1101/gad.271882.115 · DOI · Paper page
  5. Chang, 2016, Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice, Nat. Med., 22, 78, 10.1038/nm.4010 · DOI · Paper page
  6. Childs, 2016, Senescent intimal foam cells are deleterious at all stages of atherosclerosis, Science, 354, 472, 10.1126/science.aaf6659 · DOI · Paper page
  7. Chuprin, 2013, Cell fusion induced by ERVWE1 or measles virus causes cellular senescence, Genes Dev., 27, 2356, 10.1101/gad.227512.113 · DOI · Paper page
  8. Contrepois, 2017, Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression, Nat. Commun., 8, 14995, 10.1038/ncomms14995 · DOI · Paper page
  9. Cooper, 2011, Initiation of proximal-distal patterning in the vertebrate limb by signals and growth, Science, 332, 1083, 10.1126/science.1199499 · DOI
  10. Coppé, 2010, The senescence-associated secretory phenotype: the dark side of tumor suppression, Annu. Rev. Pathol., 5, 99, 10.1146/annurev-pathol-121808-102144 · DOI · Paper page
  11. Davaapil, 2017, Conserved and novel functions of programmed cellular senescence during vertebrate development, Development, 144, 106, 10.1242/dev.138222 · DOI · Paper page
  12. Dimri, 1995, A biomarker that identifies senescent human cells in culture and in aging skin in vivo, Proc. Natl. Acad. Sci. USA, 92, 9363, 10.1073/pnas.92.20.9363 · DOI · Paper page
  13. Doles, 2012, Age-associated inflammation inhibits epidermal stem cell function, Genes Dev., 26, 2144, 10.1101/gad.192294.112 · DOI · Paper page
  14. Farr, 2017, Targeting cellular senescence prevents age-related bone loss in mice, Nat. Med., 23, 1072, 10.1038/nm.4385 · DOI · Paper page
  15. Feng, 2019, CCN1-induced cellular senescence promotes heart regeneration, Circulation, 139, 2495, 10.1161/CIRCULATIONAHA.119.039530 · DOI
  16. Freund, 2010, Inflammatory networks during cellular senescence: causes and consequences, Trends Mol. Med., 16, 238, 10.1016/j.molmed.2010.03.003 · DOI · Paper page
  17. Freund, 2012, Lamin B1 loss is a senescence-associated biomarker, Mol. Biol. Cell, 23, 2066, 10.1091/mbc.e11-10-0884 · DOI · Paper page
  18. Gibaja, 2019, TGFbeta2-induced senescence during early inner ear development, Sci. Rep., 9, 5912, 10.1038/s41598-019-42040-0 · DOI
  19. Guo, 2003, Fate map of mouse ventral limb ectoderm and the apical ectodermal ridge, Dev. Biol., 264, 166, 10.1016/j.ydbio.2003.08.012 · DOI
  20. Haag, 2018, Targeting STING with covalent small-molecule inhibitors, Nature, 559, 269, 10.1038/s41586-018-0287-8 · DOI · Paper page
  21. Hayflick, 1965, The limited in vitro lifetime of human diploid cell strains, Exp. Cell Res., 37, 614, 10.1016/0014-4827(65)90211-9 · DOI · Paper page
  22. Helman, 2016, p16(Ink4a)-induced senescence of pancreatic beta cells enhances insulin secretion, Nat. Med., 22, 412, 10.1038/nm.4054 · DOI · Paper page
  23. Hesse, 2015, The human ARF tumor suppressor senses blastema activity and suppresses epimorphic tissue regeneration, eLife, 4, e07702, 10.7554/eLife.07702 · DOI
  24. Huang, 2014, Senescence-associated beta-galactosidase activity marks the visceral endoderm of mouse embryos but is not indicative of senescence, Genesis, 52, 300, 10.1002/dvg.22761 · DOI
  25. Ivanov, 2013, Lysosome-mediated processing of chromatin in senescence, J. Cell Biol., 202, 129, 10.1083/jcb.201212110 · DOI · Paper page
  26. Keyes, 2005, p63 deficiency activates a program of cellular senescence and leads to accelerated aging, Genes Dev., 19, 1986, 10.1101/gad.342305 · DOI
  27. Khattak, 2013, Germline transgenic methods for tracking cells and testing gene function during regeneration in the axolotl, Stem Cell Rep., 1, 90, 10.1016/j.stemcr.2013.03.002 · DOI
  28. Krizhanovsky, 2009, Stem cells: the promises and perils of p53, Nature, 460, 1085, 10.1038/4601085a · DOI · Paper page
  29. Krtolica, 2001, Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging, Proc. Natl. Acad. Sci. USA, 98, 12072, 10.1073/pnas.211053698 · DOI · Paper page
  30. Kuilman, 2010, The essence of senescence, Genes Dev., 24, 2463, 10.1101/gad.1971610 · DOI · Paper page
  31. Lee, 2006, Senescence-associated beta-galactosidase is lysosomal beta-galactosidase, Aging Cell, 5, 187, 10.1111/j.1474-9726.2006.00199.x · DOI · Paper page
  32. Li, 2013, Phagocyte dysfunction, tissue aging and degeneration, Ageing Res. Rev., 12, 1005, 10.1016/j.arr.2013.05.006 · DOI
  33. Li, 2009, The Ink4/Arf locus is a barrier for iPS cell reprogramming, Nature, 460, 1136, 10.1038/nature08290 · DOI · Paper page
  34. Li, 2018, Embryonic senescent cells re-enter cell cycle and contribute to tissues after birth, Cell Res., 28, 775, 10.1038/s41422-018-0050-6 · DOI · Paper page
  35. Lorda-Diez, 2015, Apoptosis during embryonic tissue remodeling is accompanied by cell senescence, Aging, 7, 974, 10.18632/aging.100844 · DOI
  36. Martínez-Zamudio, 2017, SnapShot: cellular senescence pathways, Cell, 170, 816, 10.1016/j.cell.2017.07.049 · DOI
  37. Milanovic, 2018, Senescence-associated reprogramming promotes cancer stemness, Nature, 553, 96, 10.1038/nature25167 · DOI · Paper page
  38. Nacher, 2006, The quail mesonephros: a new model for renal senescence?, J. Vasc. Res., 43, 581, 10.1159/000096076 · DOI · Paper page
  39. Ritschka, 2017, The senescence-associated secretory phenotype induces cellular plasticity and tissue regeneration, Genes Dev., 31, 172, 10.1101/gad.290635.116 · DOI · Paper page
  40. Rosello-Diez, 2011, Diffusible signals, not autonomous mechanisms, determine the main proximodistal limb subdivision, Science, 332, 1086, 10.1126/science.1199489 · DOI
  41. Sarig, 2019, Transient p53-mediated regenerative senescence in the injured heart, Circulation, 139, 2491, 10.1161/CIRCULATIONAHA.119.040125 · DOI
  42. Schmitt, 2002, A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy, Cell, 109, 335, 10.1016/S0092-8674(02)00734-1 · DOI · Paper page
  43. Sieben, 2018, Two-step senescence-focused cancer therapies, Trends Cell Biol., 28, 723, 10.1016/j.tcb.2018.04.006 · DOI · Paper page
  44. Soto-Gamez, 2017, Therapeutic interventions for aging: the case of cellular senescence, Drug Discov. Today, 22, 786, 10.1016/j.drudis.2017.01.004 · DOI · Paper page
  45. Storer, 2013, Senescence is a developmental mechanism that contributes to embryonic growth and patterning, Cell, 155, 1119, 10.1016/j.cell.2013.10.041 · DOI · Paper page
  46. Sun, 2004, Growth retardation and premature aging phenotypes in mice with disruption of the SNF2-like gene, PASG, Genes Dev., 18, 1035, 10.1101/gad.1176104 · DOI
  47. Trokovic, 2005, Fgfr1-dependent boundary cells between developing mid- and hindbrain, Dev. Biol., 278, 428, 10.1016/j.ydbio.2004.11.024 · DOI
  48. Utikal, 2009, Immortalization eliminates a roadblock during cellular reprogramming into iPS cells, Nature, 460, 1145, 10.1038/nature08285 · DOI
  49. Vasey, 2011, Spatial p21 expression profile in the mid-term mouse embryo, Transgenic Res., 20, 23, 10.1007/s11248-010-9385-6 · DOI
  50. Villiard, 2017, Senescence gives insights into the morphogenetic evolution of anamniotes, Biol. Open, 6, 891, 10.1242/bio.025809 · DOI
  51. Yang, 2017, cGAS is essential for cellular senescence, Proc. Natl. Acad. Sci. USA, 114, E4612, 10.1073/pnas.1705499114 · DOI · Paper page
  52. Yosef, 2017, p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling, EMBO J., 36, 2280, 10.15252/embj.201695553 · DOI · Paper page
  53. Zacarias-Fluck, 2015, Effect of cellular senescence on the growth of HER2-positive breast cancers, J. Natl. Cancer Inst., 107, djv020, 10.1093/jnci/djv020 · DOI
  54. Zhao, 2018, Naked mole rats can undergo developmental, oncogene-induced and DNA damage-induced cellular senescence, Proc. Natl. Acad. Sci. USA, 115, 1801, 10.1073/pnas.1721160115 · DOI
  55. Zhu, 2013, Senescent cardiac fibroblast is critical for cardiac fibrosis after myocardial infarction, PLoS ONE, 8, e74535, 10.1371/journal.pone.0074535 · DOI · Paper page

Cited by

Sorted by citations

See all 279

Metadata

Authors
Rhinn, M., Ritschka, B., & Keyes, W. M.
Affiliations
Department of Development and Stem Cells, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), 1 Rue Laurent Fries, 67404, Illkirch, France
ORCID
Keyes, William M.
Venue
Development
Publisher
The Company of Biologists
Published
2019-10-01
Volume
146
Issue
20
ISSN
  • 1477-9129
  • 0950-1991
DOI
10.1242/dev.151837
Cited by
279
References
68
Language
en
Licence
creativecommons.org/licenses/by/4.0 (vor, 496 d)
Funders
  • Fondation pour la Recherche Médicale (AJE20160635985)
  • Fondation ARC pour la Recherche sur le Cancer (PJA20181208104)
  • Université de Strasbourg (IDEX2017)
  • La Fondation Schlumberger pour l'Education et la Recherche (FSER 19)
  • Agence Nationale de la Recherche (ANR-10-LABX-0030-INRT, ANR-10-IDEX-0002-02)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review