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Molecular and Cellular Mechanisms of Apoptosis and Senescence

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1143

Special Issue Editor

Special Issue Information

Dear Colleagues,

Apoptosis and senescence are two types of cellular response to damage that are observed in different pathologies as cancer, neurodegenerative diseases and aging through different mechanisms. Cellular senescence as well as apoptosis are homeostatic processes that reduce proliferation and help to prevent the propagation of damaged cells, meaning they have an essential physiological role during development. Depending on age, the above processes could function as the main mechanisms of tumor suppression, providing an effective antitumor strategy in the early and reproductive stages of life, but both become destructive and promote aging later in life.

Given the physiological and pathological roles that apoptosis and aging may play, the study of their cellular and molecular mechanisms will be beneficial in their therapeutic exploitation.

This Special Issue calls out both original articles and reviews, providing IJMS readers with an elucidation of the understanding of the molecular and cellular mechanisms of apoptosis and aging, as well as their relationship in various pathological processes, with the aim of developing new research approaches and therapeutic strategies.

Prof. Dr. Rumiana Tzoneva
Guest Editor

Manuscript Submission Information

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Keywords

  • apoptosis
  • cellular senescence
  • cancer
  • neurodegenerative diseases

Published Papers (1 paper)

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Research

12 pages, 2770 KiB  
Article
Senescence-Associated Heterochromatin Foci Suppress γ-H2AX Focus Formation Induced by Radiation Exposure
by Takashi Oizumi, Tomoya Suzuki, Junya Kobayashi and Asako J. Nakamura
Int. J. Mol. Sci. 2024, 25(6), 3355; https://doi.org/10.3390/ijms25063355 - 15 Mar 2024
Viewed by 632
Abstract
DNA damage is induced by both endogenous and exogenous factors. Repair of DNA double-strand break (DSB), a serious damage that threatens genome stability, decreases with senescence. However, the molecular mechanisms underlying the decline in DNA repair capacity during senescence remain unclear. We performed [...] Read more.
DNA damage is induced by both endogenous and exogenous factors. Repair of DNA double-strand break (DSB), a serious damage that threatens genome stability, decreases with senescence. However, the molecular mechanisms underlying the decline in DNA repair capacity during senescence remain unclear. We performed immunofluorescence staining for phosphorylated histone H2AX (γ-H2AX) in normal human fetal lung fibroblasts and human skin fibroblasts of different ages after chronic irradiation (total dose, 1 Gy; dose rate, 1 Gy/day) to investigate the effect of cellular senescence and organismal aging on DSB repair. Accumulation of DSBs was observed with cellular senescence and organismal aging, probably caused by delayed DSB repair. Importantly, the formation of γ-H2AX foci, an early event in DSB repair, is delayed with cellular senescence and organismal aging. These results suggest that the delay in γ-H2AX focus formation might delay the overall DSB repair. Interestingly, immediate γ-H2AX foci formation was suppressed in cells with senescence-associated heterochromatin foci (SAHF). To investigate the relationship between the γ-H2AX focus formation and SAHF, we used LiCl to relax the SAHFs, followed by irradiation. We demonstrated that LiCl rescued the delayed γ-H2AX foci formation associated with cellular senescence. This indicates that SAHF interferes with γ-H2AX focus formation and inhibits DSB repair in radiation-induced DSB. Our results suggest that therapeutic targeting of SAHFs have potential to resolve DSB repair dysfunction associated with cellular senescence. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Apoptosis and Senescence)
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