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Molecular and Cellular Mechanisms of Apoptosis and Senescence
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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: closed (20 January 2025) | Viewed by 9117

Special Issue Editor

Prof. Dr. Rumiana Tzoneva

E-Mail Website
Guest Editor
Laboratory of Transmembrane Signaling, Institute of Biophysics and Biomedical Engineering Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria
Interests: cell biology; antioxidants; transmembrane signalisation; actin cytoskeleton; anti-tumor therapy; cytotoxicity; apoptosis
Special Issues, Collections and Topics in MDPI journals

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

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • apoptosis
  • cellular senescence
  • cancer
  • neurodegenerative diseases

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Published Papers (5 papers)

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Research

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18 pages, 6344 KiB  
Article
Spatio-Temporal Characterization of Cellular Senescence Hallmarks in Experimental Ischemic Stroke
by Júlia Baixauli-Martín, Maria Consuelo Burguete, Mikahela A. López-Morales, María Castelló-Ruiz, Alicia Aliena-Valero, Teresa Jover-Mengual, Dianoush Falahatgaroshibi, Germán Torregrosa and Juan B. Salom
Int. J. Mol. Sci. 2025, 26(5), 2364; https://doi.org/10.3390/ijms26052364 - 6 Mar 2025
Viewed by 679
Abstract
In recent years, evidence of the existence of cellular senescence in the central nervous system has accumulated. In ischemic stroke, cellular senescence has been suggested as an unidentified pathophysiological mechanism, prompting research into the neuroprotective potential of senolytic drugs. This study aims to [...] Read more.
In recent years, evidence of the existence of cellular senescence in the central nervous system has accumulated. In ischemic stroke, cellular senescence has been suggested as an unidentified pathophysiological mechanism, prompting research into the neuroprotective potential of senolytic drugs. This study aims to provide spatio-temporal evidence of the existence of brain senescence following ischemic stroke and to elucidate the involved pathways and cell types. We focused on the most established markers of senescence: cell cycle arrest (p16, p21); lysosomal activity (senescence-associated β-galactosidase [SA-β-gal]); the senescence-associated secretory phenotype ([SASP]; Interleukin-6 [IL-6], Interleukin-1β [IL-1β], Tumor necrosis factor [TNF]); and DNA/nuclear damage (Checkpoint kinase 1 [Chk1], Checkpoint kinase 2 [Chk2], Lamin B1 [LB1]). Male Wistar rats underwent 60 min of transient middle cerebral artery occlusion, followed by 24 h and 3, 7, and 14 days of recovery. Our results show significant increases in p16 expression, particularly in neurons and microglia/macrophages; SA-β-gal accumulation in the infarcted tissue; significant increases in SASP markers as early as 24 h after reperfusion; and significant changes in Chk1, Chk2, and LB1 at 14 days. Overall, our findings lend support to the existence of senescence after ischemic stroke in neurons and microglia/macrophages. However, there is still room to gain further insight into the role of senescence in the pathophysiology of ischemic stroke and in the implementation of successful senolytic therapy. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Apoptosis and Senescence)
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10 pages, 2115 KiB  
Article
HMGA1 Plays a Role in Counteracting DNA Damage Induced by BoHV-1 Productive Infection
by Heci Zhao, Xiaotian Fu, Xiuyan Ding and Liqian Zhu
Int. J. Mol. Sci. 2024, 25(24), 13265; https://doi.org/10.3390/ijms252413265 - 10 Dec 2024
Viewed by 830
Abstract
Bovine herpesvirus 1 (BoHV-1) productive infection induces the generation of DNA double-strand breaks (DSBs), which may consequently lead to cell apoptosis. In response to DSBs, the DNA damage repair-related protein 53BP1 is recruited to the sites of DSBs, leading to the formation of [...] Read more.
Bovine herpesvirus 1 (BoHV-1) productive infection induces the generation of DNA double-strand breaks (DSBs), which may consequently lead to cell apoptosis. In response to DSBs, the DNA damage repair-related protein 53BP1 is recruited to the sites of DSBs, leading to the formation of 53BP1foci, which are crucial for the repair of damaged DNA and maintaining genomic integrity by repairing DSBs. In this study, we discovered that HMGA1 may play a significant role in counteracting virus infection-induced DNA damage, as the siRNA-mediated knockdown of HMGA1 protein expression or inhibition of HMGA1 activity by the chemical inhibitor Netropsin uniformly exacerbates the DNA damage induced by BoHV-1 productive infection. Interestingly, HMGA1 may positively regulate 53BP1 expression, and treatment with Netropsin reduced the accumulation of 53BP1 protein in the nucleus, suggesting that HMGA1 may potentially influence 53BP1’s nuclear localization. However, this effect was reversed in the context of virus infection. Furthermore, Netropsin treatment restored the disruption of 53BP1 foci caused by virus infection, which is consistent with our findings that Netropsin enhances the nuclear accumulation of 53BP1. Collectively, these results indicate that HMGA1 is involved in countering DNA damage induced by virus infection. HMGA1 does indeed modulate the nuclear accumulation of 53BP1 protein, but this effect is counteracted by virus infection. Therefore, the biological function of HMGA1 in countering virus infection-induced DNA damage may be independent of its regulation of 53BP1 signaling. This is the first report suggesting that HMGA1 may be implicated in virus infection-induced DNA damage, although the precise mechanism remains to be elucidated. Furthermore, we report for the first time an interaction between HMGA1 and 53BP1, which is disrupted following virus infection. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Apoptosis and Senescence)
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12 pages, 1718 KiB  
Article
Melatonin Supplementation Alleviates Impaired Spatial Memory by Influencing Aβ1-42 Metabolism via γ-Secretase in the icvAβ1-42 Rat Model with Pinealectomy
by Irina Georgieva, Jana Tchekalarova, Zlatina Nenchovska, Lidia Kortenska and Rumiana Tzoneva
Int. J. Mol. Sci. 2024, 25(19), 10294; https://doi.org/10.3390/ijms251910294 - 24 Sep 2024
Cited by 2 | Viewed by 1598
Abstract
In the search for Alzheimer’s disease (AD) therapies, most animal models focus on familial AD, which accounts for a small fraction of cases. The majority of AD cases arise from stress factors, such as oxidative stress, leading to neurological changes (sporadic AD). Early [...] Read more.
In the search for Alzheimer’s disease (AD) therapies, most animal models focus on familial AD, which accounts for a small fraction of cases. The majority of AD cases arise from stress factors, such as oxidative stress, leading to neurological changes (sporadic AD). Early in AD progression, dysfunction in γ-secretase causes the formation of insoluble Aβ1-42 peptides, which aggregate into senile plaques, triggering neurodegeneration, cognitive decline, and circadian rhythm disturbances. To better model sporadic AD, we used a new AD rat model induced by intracerebroventricular administration of Aβ1-42 oligomers (icvAβ1-42) combined with melatonin deficiency via pinealectomy (pin). We validated this model by assessing spatial memory using the radial arm maze test and measuring Aβ1-42 and γ-secretase levels in the frontal cortex and hippocampus with ELISA. The icvAβ1-42 + pin model experienced impaired spatial memory and increased Aβ1-42 and γ-secretase levels in the frontal cortex and hippocampus, effects not seen with either icvAβ1-42 or the pin alone. Chronic melatonin treatment reversed memory deficits and reduced Aβ1-42 and γ-secretase levels in both structures. Our findings suggest that our icvAβ1-42 + pin model is extremely valuable for future AD research. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Apoptosis and Senescence)
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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
Cited by 3 | Viewed by 2495
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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Review

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26 pages, 2406 KiB  
Review
Paraptosis—A Distinct Pathway to Cell Death
by Claudia Kunst, Deniz Tümen, Martha Ernst, Hauke Christian Tews, Martina Müller and Karsten Gülow
Int. J. Mol. Sci. 2024, 25(21), 11478; https://doi.org/10.3390/ijms252111478 - 25 Oct 2024
Cited by 2 | Viewed by 2273
Abstract
Cell death is a critical biological process necessary for development, tissue maintenance, and defense against diseases. To date, more than 20 forms of cell death have been identified, each defined by unique molecular pathways. Understanding these different forms of cell death is essential [...] Read more.
Cell death is a critical biological process necessary for development, tissue maintenance, and defense against diseases. To date, more than 20 forms of cell death have been identified, each defined by unique molecular pathways. Understanding these different forms of cell death is essential for investigating the pathogenesis of diseases such as cancer, neurodegenerative disorders, and autoimmune conditions and developing appropriate therapies. Paraptosis is a distinct form of regulated cell death characterized by cytoplasmic vacuolation and dilatation of cellular organelles like the mitochondria and endoplasmic reticulum (ER). It is regulated by several signaling pathways, for instance, those associated with ER stress, calcium overload, oxidative stress, and specific cascades such as insulin-like growth factor I receptor (IGF-IR) and its downstream signaling pathways comprising mitogen-activated protein kinases (MAPKs) and Jun N-terminal kinase (JNK). Paraptosis has been observed in diverse biological contexts, including development and cellular stress responses in neuronal, retinal, endothelial, and muscle cells. The induction of paraptosis is increasingly important in anticancer therapy, as it targets non-apoptotic stress responses in tumor cells, which can be utilized to induce cell death. This approach enhances treatment efficacy and addresses drug resistance, particularly in cases where cancer cells are resistant to apoptosis. Combining paraptosis-inducing agents with traditional therapies holds promise for enhancing treatment efficacy and overcoming drug resistance, suggesting a valuable strategy in anticancer therapy. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Apoptosis and Senescence)
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