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Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer

Overlapping risks for cancer and cardiovascular diseases (CVD), the two leading causes of mortality worldwide, suggest a shared biology between these diseases. The role of senescence in the development of cancer and CVD has been established. However, its role as the intersection between these diseas...

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Autores principales: Banerjee, Priyanka, Kotla, Sivareddy, Reddy Velatooru, Loka, Abe, Rei J., Davis, Elizabeth A., Cooke, John P., Schadler, Keri, Deswal, Anita, Herrmann, Joerg, Lin, Steven H., Abe, Jun-ichi, Le, Nhat-Tu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8563837/
https://www.ncbi.nlm.nih.gov/pubmed/34746270
http://dx.doi.org/10.3389/fcvm.2021.763930
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author Banerjee, Priyanka
Kotla, Sivareddy
Reddy Velatooru, Loka
Abe, Rei J.
Davis, Elizabeth A.
Cooke, John P.
Schadler, Keri
Deswal, Anita
Herrmann, Joerg
Lin, Steven H.
Abe, Jun-ichi
Le, Nhat-Tu
author_facet Banerjee, Priyanka
Kotla, Sivareddy
Reddy Velatooru, Loka
Abe, Rei J.
Davis, Elizabeth A.
Cooke, John P.
Schadler, Keri
Deswal, Anita
Herrmann, Joerg
Lin, Steven H.
Abe, Jun-ichi
Le, Nhat-Tu
author_sort Banerjee, Priyanka
collection PubMed
description Overlapping risks for cancer and cardiovascular diseases (CVD), the two leading causes of mortality worldwide, suggest a shared biology between these diseases. The role of senescence in the development of cancer and CVD has been established. However, its role as the intersection between these diseases remains unclear. Senescence was originally characterized by an irreversible cell cycle arrest after a high number of divisions, namely replicative senescence (RS). However, it is becoming clear that senescence can also be instigated by cellular stress, so-called stress-induced premature senescence (SIPS). Telomere shortening is a hallmark of RS. The contribution of telomere DNA damage and subsequent DNA damage response/repair to SIPS has also been suggested. Although cellular senescence can mediate cell cycle arrest, senescent cells can also remain metabolically active and secrete cytokines, chemokines, growth factors, and reactive oxygen species (ROS), so-called senescence-associated secretory phenotype (SASP). The involvement of SASP in both cancer and CVD has been established. In patients with cancer or CVD, SASP is induced by various stressors including cancer treatments, pro-inflammatory cytokines, and ROS. Therefore, SASP can be the intersection between cancer and CVD. Importantly, the conventional concept of senescence as the mediator of cell cycle arrest has been challenged, as it was recently reported that chemotherapy-induced senescence can reprogram senescent cancer cells to acquire “stemness” (SAS: senescence-associated stemness). SAS allows senescent cancer cells to escape cell cycle arrest with strongly enhanced clonogenic growth capacity. SAS supports senescent cells to promote both cancer and CVD, particularly in highly stressful conditions such as cancer treatments, myocardial infarction, and heart failure. As therapeutic advances have increased overlapping risk factors for cancer and CVD, to further understand their interaction may provide better prevention, earlier detection, and safer treatment. Thus, it is critical to study the mechanisms by which these senescence pathways (SAS/SASP) are induced and regulated in both cancer and CVD.
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spelling pubmed-85638372021-11-04 Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer Banerjee, Priyanka Kotla, Sivareddy Reddy Velatooru, Loka Abe, Rei J. Davis, Elizabeth A. Cooke, John P. Schadler, Keri Deswal, Anita Herrmann, Joerg Lin, Steven H. Abe, Jun-ichi Le, Nhat-Tu Front Cardiovasc Med Cardiovascular Medicine Overlapping risks for cancer and cardiovascular diseases (CVD), the two leading causes of mortality worldwide, suggest a shared biology between these diseases. The role of senescence in the development of cancer and CVD has been established. However, its role as the intersection between these diseases remains unclear. Senescence was originally characterized by an irreversible cell cycle arrest after a high number of divisions, namely replicative senescence (RS). However, it is becoming clear that senescence can also be instigated by cellular stress, so-called stress-induced premature senescence (SIPS). Telomere shortening is a hallmark of RS. The contribution of telomere DNA damage and subsequent DNA damage response/repair to SIPS has also been suggested. Although cellular senescence can mediate cell cycle arrest, senescent cells can also remain metabolically active and secrete cytokines, chemokines, growth factors, and reactive oxygen species (ROS), so-called senescence-associated secretory phenotype (SASP). The involvement of SASP in both cancer and CVD has been established. In patients with cancer or CVD, SASP is induced by various stressors including cancer treatments, pro-inflammatory cytokines, and ROS. Therefore, SASP can be the intersection between cancer and CVD. Importantly, the conventional concept of senescence as the mediator of cell cycle arrest has been challenged, as it was recently reported that chemotherapy-induced senescence can reprogram senescent cancer cells to acquire “stemness” (SAS: senescence-associated stemness). SAS allows senescent cancer cells to escape cell cycle arrest with strongly enhanced clonogenic growth capacity. SAS supports senescent cells to promote both cancer and CVD, particularly in highly stressful conditions such as cancer treatments, myocardial infarction, and heart failure. As therapeutic advances have increased overlapping risk factors for cancer and CVD, to further understand their interaction may provide better prevention, earlier detection, and safer treatment. Thus, it is critical to study the mechanisms by which these senescence pathways (SAS/SASP) are induced and regulated in both cancer and CVD. Frontiers Media S.A. 2021-10-20 /pmc/articles/PMC8563837/ /pubmed/34746270 http://dx.doi.org/10.3389/fcvm.2021.763930 Text en Copyright © 2021 Banerjee, Kotla, Reddy Velatooru, Abe, Davis, Cooke, Schadler, Deswal, Herrmann, Lin, Abe and Le. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cardiovascular Medicine
Banerjee, Priyanka
Kotla, Sivareddy
Reddy Velatooru, Loka
Abe, Rei J.
Davis, Elizabeth A.
Cooke, John P.
Schadler, Keri
Deswal, Anita
Herrmann, Joerg
Lin, Steven H.
Abe, Jun-ichi
Le, Nhat-Tu
Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title_full Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title_fullStr Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title_full_unstemmed Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title_short Senescence-Associated Secretory Phenotype as a Hinge Between Cardiovascular Diseases and Cancer
title_sort senescence-associated secretory phenotype as a hinge between cardiovascular diseases and cancer
topic Cardiovascular Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8563837/
https://www.ncbi.nlm.nih.gov/pubmed/34746270
http://dx.doi.org/10.3389/fcvm.2021.763930
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