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Senopathies—Diseases Associated with Cellular Senescence

Cellular senescence describes a stable cell cycle arrest state with a characteristic phenotype. Senescent cells accumulate in the human body during normal aging, limiting the lifespan and promoting aging-related, but also several non-related, pathologies. We propose to refer to all diseases whose pa...

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Detalles Bibliográficos
Autores principales: Lushchak, Oleh, Schosserer, Markus, Grillari, Johannes
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10296713/
https://www.ncbi.nlm.nih.gov/pubmed/37371545
http://dx.doi.org/10.3390/biom13060966
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author Lushchak, Oleh
Schosserer, Markus
Grillari, Johannes
author_facet Lushchak, Oleh
Schosserer, Markus
Grillari, Johannes
author_sort Lushchak, Oleh
collection PubMed
description Cellular senescence describes a stable cell cycle arrest state with a characteristic phenotype. Senescent cells accumulate in the human body during normal aging, limiting the lifespan and promoting aging-related, but also several non-related, pathologies. We propose to refer to all diseases whose pathogenesis or progression is associated with cellular senescence as “senopathies”. Targeting senescent cells with senolytics or senomorphics is likely to mitigate these pathologies. Examples of senopathies include cardiovascular, metabolic, musculoskeletal, liver, kidney, and lung diseases and neurodegeneration. For all these pathologies, animal studies provide clear mechanistic evidence for a connection between senescent cell accumulation and disease progression. The major persisting challenge in developing novel senotherapies is the heterogeneity of senescence phenotypes, causing a lack of universal biomarkers and difficulties in discriminating senescent from non-senescent cells.
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spelling pubmed-102967132023-06-28 Senopathies—Diseases Associated with Cellular Senescence Lushchak, Oleh Schosserer, Markus Grillari, Johannes Biomolecules Opinion Cellular senescence describes a stable cell cycle arrest state with a characteristic phenotype. Senescent cells accumulate in the human body during normal aging, limiting the lifespan and promoting aging-related, but also several non-related, pathologies. We propose to refer to all diseases whose pathogenesis or progression is associated with cellular senescence as “senopathies”. Targeting senescent cells with senolytics or senomorphics is likely to mitigate these pathologies. Examples of senopathies include cardiovascular, metabolic, musculoskeletal, liver, kidney, and lung diseases and neurodegeneration. For all these pathologies, animal studies provide clear mechanistic evidence for a connection between senescent cell accumulation and disease progression. The major persisting challenge in developing novel senotherapies is the heterogeneity of senescence phenotypes, causing a lack of universal biomarkers and difficulties in discriminating senescent from non-senescent cells. MDPI 2023-06-08 /pmc/articles/PMC10296713/ /pubmed/37371545 http://dx.doi.org/10.3390/biom13060966 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Opinion
Lushchak, Oleh
Schosserer, Markus
Grillari, Johannes
Senopathies—Diseases Associated with Cellular Senescence
title Senopathies—Diseases Associated with Cellular Senescence
title_full Senopathies—Diseases Associated with Cellular Senescence
title_fullStr Senopathies—Diseases Associated with Cellular Senescence
title_full_unstemmed Senopathies—Diseases Associated with Cellular Senescence
title_short Senopathies—Diseases Associated with Cellular Senescence
title_sort senopathies—diseases associated with cellular senescence
topic Opinion
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10296713/
https://www.ncbi.nlm.nih.gov/pubmed/37371545
http://dx.doi.org/10.3390/biom13060966
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