CoChat
Sign Up
Cited by 71

The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.

The Emergence of Senescent Surface Biomarkers as Senotherapeutic Targets

Rossi, Martina, Abdelmohsen, Kotb·2021·Cells
DOI 10.3390/cells10071740PMC PMC8305747
Open this paper in CoChat — free account

Abstract

Senescence is linked to a wide range of age-associated diseases and physiological declines. Thus, senotherapeutics are emerging to suppress the detrimental effects of senescence either by senomorphics or senolytics. Senomorphics suppress the traits associated with senescence phenotypes, while senolytics aim to clear senescent cells by suppressing their survival and enhancing the apoptotic pathways. The main goal of these approaches is to suppress the proinflammatory senescence-associated secretory phenotype (SASP) and to promote the immune recognition and elimination of senescent cells. One increasingly attractive approach is the targeting of molecules or proteins specifically present on the surface of senescent cells. These proteins may play roles in the maintenance and survival of senescent cells and hence can be targeted for senolysis. In this review, we summarize the recent knowledge regarding senolysis with a focus on novel surface biomarkers of cellular senescence and discuss their emergence as senotherapeutic targets.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/cells10071740

Cites

24 of 24 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • New senolytic vulnerabilities include the p21CIP1 pathway, novel SnC surface markers revealed through transcriptomic profiling, and distinctive metabolic dependencies such as glutaminolysis.

    “These include the p21CIP1 pathway125, novel SnC surface markers revealed through transcriptomic profiling, and distinctive metabolic dependencies such as glutaminolysis126.”

    From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [126]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 64

  1. 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
  2. Kuilman, 2010, The Essence of Senescence, Genes Dev., 24, 2463, 10.1101/gad.1971610 · DOI · Paper page
  3. Nehme, 2018, Hallmarks of Cellular Senescence, Trends Cell Biol., 28, 436, 10.1016/j.tcb.2018.02.001 · DOI · Paper page
  4. Terzi, 2016, The Cell Fate: Senescence or Quiescence, Mol. Biol. Rep., 43, 1213, 10.1007/s11033-016-4065-0 · DOI · Paper page
  5. He, 2017, Senescence in Health and Disease, Cell, 169, 1000, 10.1016/j.cell.2017.05.015 · DOI · Paper page
  6. 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
  7. Franceschi, 2014, Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases, J. Gerontol. A Biol. Sci. Med. Sci., 69, S4, 10.1093/gerona/glu057 · DOI · Paper page
  8. McHugh, 2018, Senescence and Aging: Causes, Consequences, and Therapeutic Avenues, J. Cell Biol., 217, 65, 10.1083/jcb.201708092 · DOI · Paper page
  9. Druelle, 2016, ATF6α Regulates Morphological Changes Associated with Senescence in Human Fibroblasts, Oncotarget, 7, 67699, 10.18632/oncotarget.11505 · DOI · Paper page
  10. Freund, 2012, Lamin B1 Loss Is a Senescence-Associated Biomarker, Mol. Biol. Cell, 23, 2066, 10.1091/mbc.e11-10-0884 · DOI · Paper page
  11. 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
  12. Itahana, 2013, Colorimetric Detection of Senescence-Associated β Galactosidase, Methods Mol. Biol., 965, 143, 10.1007/978-1-62703-239-1_8 · DOI
  13. Kim, 2019, Mitochondrial Protection Partly Mitigates Kidney Cellular Senescence in Swine Atherosclerotic Renal Artery Stenosis, Cell. Physiol. Biochem., 52, 617, 10.33594/000000044 · DOI
  14. Desprez, 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
  15. Rea, 2018, Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines, Front. Immunol., 9, 586, 10.3389/fimmu.2018.00586 · DOI · Paper page
  16. Kadota, 2018, Emerging Role of Extracellular Vesicles as a Senescence-Associated Secretory Phenotype: Insights into the Pathophysiology of Lung Diseases, Mol. Aspects Med., 60, 92, 10.1016/j.mam.2017.11.005 · DOI
  17. Kuo, 2008, Gamma-H2AX—A Novel Biomarker for DNA Double-Strand Breaks, In Vivo, 22, 305
  18. Rodier, 2011, DNA-SCARS: Distinct Nuclear Structures That Sustain Damage-Induced Senescence Growth Arrest and Inflammatory Cytokine Secretion, J. Cell Sci., 124, 68, 10.1242/jcs.071340 · DOI · Paper page
  19. Zhang, 2007, Molecular Dissection of Formation of Senescence-Associated Heterochromatin Foci, Mol. Cell Biol., 27, 2343, 10.1128/MCB.02019-06 · DOI · Paper page
  20. Aird, 2013, Detection of Senescence-Associated Heterochromatin Foci (SAHF), Methods Mol. Biol., 965, 185, 10.1007/978-1-62703-239-1_12 · DOI
  21. Rufini, 2013, Senescence and Aging: The Critical Roles of P53, Oncogene, 32, 5129, 10.1038/onc.2012.640 · DOI · Paper page
  22. Sammons, 2020, Tumor Suppressor P53: From Engaging DNA to Target Gene Regulation, Nucleic Acids Res., 48, 8848, 10.1093/nar/gkaa666 · DOI
  23. 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
  24. Weichhart, 2018, MTOR as Regulator of Lifespan, Aging, and Cellular Senescence: A Mini-Review, Gerontology, 64, 127, 10.1159/000484629 · DOI · Paper page
  25. Payea, M.J., Anerillas, C., Tharakan, R., and Gorospe, M. (2021). Translational Control during Cellular Senescence. Mol. Cell Biol., 41. · DOI
  26. Kany, S., Vollrath, J.T., and Relja, B. (2019). Cytokines in Inflammatory Disease. Int. J. Mol. Sci., 20. · DOI
  27. Idda, 2020, Survey of Senescent Cell Markers with Age in Human Tissues, Aging, 12, 4052, 10.18632/aging.102903 · DOI · Paper page
  28. Burd, 2013, Monitoring Tumorigenesis and Senescence in Vivo with a P16(INK4a)-Luciferase Model, Cell, 152, 340, 10.1016/j.cell.2012.12.010 · DOI · Paper page
  29. Muñoz-Espin, D., and Demaria, M. (2020). Targeted Senolytic Strategies Based on the Senescent Surfaceome. Senolytics in Disease, Ageing and Longevity, Springer International Publishing. · DOI
  30. Muñoz-Espin, D., and Demaria, M. (2020). Senolysis and Senostasis Through the Plasma Membrane. Senolytics in Disease, Ageing and Longevity, Springer International Publishing. · DOI
  31. 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
  32. Li, 2018, LncRNA-OIS1 Regulates DPP4 Activation to Modulate Senescence Induced by RAS, Nucleic Acids Res., 46, 4213, 10.1093/nar/gky087 · DOI
  33. Johmura, 2021, Senolysis by Glutaminolysis Inhibition Ameliorates Various Age-Associated Disorders, Science, 371, 265, 10.1126/science.abb5916 · DOI · Paper page
  34. Chen, 2020, Dipeptidyl Peptidase-4 Inhibition Improves Endothelial Senescence by Activating AMPK/SIRT1/Nrf2 Signaling Pathway, Biochem. Pharmacol., 177, 113951, 10.1016/j.bcp.2020.113951 · DOI · Paper page
  35. Worthen, 2020, CD26 Identifies a Subpopulation of Fibroblasts That Produce the Majority of Collagen during Wound Healing in Human Skin, J. Investig. Dermatol., 140, 2515, 10.1016/j.jid.2020.04.010 · DOI
  36. Wang, 2021, Targeting Cellular Senescence Prevents Glucocorticoid-Induced Bone Loss through Modulation of the DPP4-GLP-1 Axis, Signal Transduct Target Ther., 6, 143, 10.1038/s41392-021-00528-0 · DOI
  37. Kim, 2018, SCAMP4 Enhances the Senescent Cell Secretome, Genes Dev., 32, 909, 10.1101/gad.313270.118 · DOI
  38. Zingoni, 2015, Genotoxic Stress Induces Senescence-Associated ADAM10-Dependent Release of NKG2D MIC Ligands in Multiple Myeloma Cells, J. Immunol., 195, 736, 10.4049/jimmunol.1402643 · DOI
  39. Madsen, 2017, Decoy TRAIL Receptor CD264: A Cell Surface Marker of Cellular Aging for Human Bone Marrow-Derived Mesenchymal Stem Cells, Stem Cell Res. Ther., 8, 201, 10.1186/s13287-017-0649-4 · DOI
  40. Cui, 2013, Notch3 Functions as a Tumor Suppressor by Controlling Cellular Senescence, Cancer Res., 73, 3451, 10.1158/0008-5472.CAN-12-3902 · DOI
  41. Chong, 2018, CD36 Initiates the Secretory Phenotype during the Establishment of Cellular Senescence, EMBO Rep., 19, e45274, 10.15252/embr.201745274 · DOI
  42. Frescas, 2017, Senescent Cells Expose and Secrete an Oxidized Form of Membrane-Bound Vimentin as Revealed by a Natural Polyreactive Antibody, Proc. Natl. Acad. Sci USA, 114, E1668, 10.1073/pnas.1614661114 · DOI · Paper page
  43. Lioulios, 2021, T Cell Markers Recount the Course of Immunosenescence in Healthy Individuals and Chronic Kidney Disease, Clin. Immunol., 225, 108685, 10.1016/j.clim.2021.108685 · DOI
  44. Aung, K.T., Akiyama, K., Kunitomo, M., Mun, A.Y., Tosa, I., Nguyen, H.T.T., Zhang, J., Kohno, T., Ono, M., and Hara, E.S. (2020). Aging-Affected MSC Functions and Severity of Periodontal Tissue Destruction in a Ligature-Induced Mouse Periodontitis Model. Int. J. Mol. Sci., 21. · DOI
  45. Harada, 2021, FZD5 Regulates Cellular Senescence in Human Mesenchymal Stem/Stromal Cells, Stem Cells, 39, 318, 10.1002/stem.3317 · DOI
  46. Nielson, 2017, Identification of Hip BMD Loss and Fracture Risk Markers Through Population-Based Serum Proteomics, J. Bone Miner. Res., 32, 1559, 10.1002/jbmr.3125 · DOI
  47. Qu, 2020, An NIR-Responsive DNA-Mediated Nanotetrahedron Enhances the Clearance of Senescent Cells, Adv. Mater., 32, e2000184, 10.1002/adma.202000184 · DOI
  48. Lizardo, 2017, Regulation of Lipids Is Central to Replicative Senescence, Mol. Biosyst., 13, 498, 10.1039/C6MB00842A · DOI
  49. Chia, 2008, Incretin-Based Therapies in Type 2 Diabetes Mellitus, J. Clin. Endocrinol. Metab., 93, 3703, 10.1210/jc.2007-2109 · DOI
  50. Schmitz, 2004, GLP-1 Receptor Agonists and DPP-4 Inhibitors in the Treatment of Type 2 Diabetes, Horm. Metab. Res., 36, 867, 10.1055/s-2004-826178 · DOI
  51. Munk, R., Kim, K.M., Gorospe, M., and Abdelmohsen, K. (2019). Senescence LncRNAs Govern Cell Surface Components: LncRNA-OIS1 Transcriptionally Elevates DPP4. Non Coding RNA Investig., 3. · DOI
  52. Xin, 2019, Dipeptidyl Peptidase-4 Inhibition Prevents Vascular Aging in Mice under Chronic Stress: Modulation of Oxidative Stress and Inflammation, Chem. Biol. Interact., 314, 108842, 10.1016/j.cbi.2019.108842 · DOI
  53. Ban, 2020, Renoprotective Effect of a Dipeptidyl Peptidase-4 Inhibitor on Aging Mice, Aging Dis., 11, 588, 10.14336/AD.2019.0620 · DOI
  54. Dave, 2013, Differential Expression of CD148 on Leukocyte Subsets in Inflammatory Arthritis, Arthritis Res. Ther., 15, R108, 10.1186/ar4288 · DOI
  55. Zhu, 2011, Receptor-like Tyrosine Phosphatases CD45 and CD148 Have Distinct Functions in Chemoattractant-Mediated Neutrophil Migration and Response to S. Aureus, Immunity, 35, 757, 10.1016/j.immuni.2011.09.011 · DOI
  56. Takahashi, 2020, Agonistic Anti-CD148 Monoclonal Antibody Attenuates Diabetic Nephropathy in Mice, Am. J. Physiol. Renal Physiol., 318, F647, 10.1152/ajprenal.00288.2019 · DOI
  57. Orjalo, 2009, Cell Surface-Bound IL-1alpha Is an Upstream Regulator of the Senescence-Associated IL-6/IL-8 Cytokine Network, Proc. Natl. Acad. Sci. USA, 106, 17031, 10.1073/pnas.0905299106 · DOI · Paper page
  58. Kim, 2019, Senotherapeutics: Emerging Strategy for Healthy Aging and Age-Related Disease, BMB Rep., 52, 47, 10.5483/BMBRep.2019.52.1.293 · DOI
  59. 2019, Targeting Senescent Cells: Approaches, Opportunities, Challenges, Aging, 11, 12844, 10.18632/aging.102557 · DOI
  60. Roos, 2016, Chronic Senolytic Treatment Alleviates Established Vasomotor Dysfunction in Aged or Atherosclerotic Mice, Aging Cell, 15, 973, 10.1111/acel.12458 · DOI · Paper page
  61. Farr, 2017, Targeting Cellular Senescence Prevents Age-Related Bone Loss in Mice, Nat. Med., 23, 1072, 10.1038/nm.4385 · DOI · Paper page
  62. 2020, First Evidence That Senolytics Are Effective at Decreasing Senescent Cells in Humans, EBioMedicine, 56, 102473, 10.1016/j.ebiom.2019.09.053 · DOI
  63. Thompson, 2019, Targeted Elimination of Senescent Beta Cells Prevents Type 1 Diabetes, Cell Metab., 29, 1045, 10.1016/j.cmet.2019.01.021 · DOI · Paper page
  64. Caruana, 2014, From Monoclonal Antibodies to Chimeric Antigen Receptors for the Treatment of Human Malignancies, Semin. Oncol., 41, 661, 10.1053/j.seminoncol.2014.08.005 · DOI

Cited by

Sorted by citations

Metadata

Authors
Rossi, M., & Abdelmohsen, K.
Venue
Cells
Publisher
MDPI AG
Published
2021-07-09
Volume
10
Issue
7
Pages
1740
ISSN
2073-4409
DOI
10.3390/cells10071740
PMC
PMC8305747
Cited by
71
References
24
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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