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Biology
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Mechanisms of Cellular Senescence in Aging and Age-Related Diseases
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Mechanisms of Cellular Senescence in Aging and Age-Related Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 3958

Special Issue Editors

Dr. Giulia Matacchione

E-Mail Website
Guest Editor
Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, 60126 Ancona, Italy
Interests: aging; cellular senescence; age-related diseases; circulating biomarkers; immunosenescence; inflammaging
Special Issues, Collections and Topics in MDPI journals
Dr. Deborah Ramini

E-Mail Website
Guest Editor
IRCCS INRCA, 60121 Ancona, Italy
Interests: aging; cellular senescence; cellular models; extracellular vesicles; nucleic acids

Special Issue Information

Dear Colleagues, 

As the population is progressively aging and this phenomenon is accompanied by an increased incidence of age-related diseases (ARDs), the discovery of mechanisms to decelerate the aging process and postpone the development of the most common ARDs has become of widespread interest.

Inflammaging is the systemic, low-grade, inflammatory status associated with aging, which is considered a shared risk factor for the most common ARDs. The increased burden of senescent cells (SCs) is recognized as a key player in promoting inflammaging since SCs are characterized by the acquisition of a senescence-associated secretory phenotype (SASP) with proinflammatory activity. SASP, which is fueled by the DNA damage response (DDR), is characterized by NF-kB and NLRP3 inflammasome pathways activation, and by the consequent synthesis and release of a plethora of proinflammatory factors such as interleukins, chemokines, growth factors, matrix-degrading enzymes, reactive oxygen species and non-coding RNA, i.e., miRNAs.

The aim of this Special Issue is to convey the current understanding of cellular senescence and inflammaging and their role in aging and age-related diseases, as well as to investigate recent advancements in the field and provide an overview of senolytics/ senomorphics treatment as a potential therapy in age-related diseases. Original reviews and research articles are welcome.

We look forward to receiving your contributions.

Dr. Giulia Matacchione
Dr. Deborah Ramini
Guest Editors

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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • cellular senescence
  • age-related diseases
  • aging
  • senolytics
  • senomorphics
  • biomarkers
  • immunosenescence
  • inflammaging
  • SASP

Published Papers (2 papers)

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Research

13 pages, 2393 KiB  
Article
Zingiber officinale Roscoe Rhizome Extract Exerts Senomorphic and Anti-Inflammatory Activities on Human Endothelial Cells
by Giulia Matacchione, Vittoria Borgonetti, Deborah Ramini, Andrea Silvestrini, Marta Ojetti, Nicoletta Galeotti and Fabiola Olivieri
Biology 2023, 12(3), 438; https://doi.org/10.3390/biology12030438 - 12 Mar 2023
Cited by 1 | Viewed by 1767
Abstract
Aging is related to a low-grade and sterile inflammation called inflammaging, recognized as the main risk factor for age-related disease (ARD) development. Inflammaging is fostered by the repeated activation of immune cells, as well as by the accumulation of senescent cells. Recently, a [...] Read more.
Aging is related to a low-grade and sterile inflammation called inflammaging, recognized as the main risk factor for age-related disease (ARD) development. Inflammaging is fostered by the repeated activation of immune cells, as well as by the accumulation of senescent cells. Recently, a number of natural compounds have gained attention to be tested as anti-aging therapies, based on their anti-inflammatory activity and/or ability to reduce the pro-inflammatory secretome of senescent cells (senomorphyc activity). Here, we investigated the anti-inflammatory and senomorphic properties of an Asian-native Zingiber officinale Roscoe extract (ZOE), commonly consumed as a food spice and herbal medicine. We employed two models of primary endothelial cells (HUVECs), such as the replicative-senescence and LPS-induced response, to investigate the anti-inflammatory/senomorphic effect of ZOE, and one cellular model of neuroinflammation, i.e., immortalized murine microglial cells (BV2). First, we found that the ZOE treatment induced the inhibition of NF-kB activation in BV2 cells. Among the constituents of ZOE, we showed that the terpenoid-enriched fraction (ZTE) was the component able to counteract the phosphorylation of NF-kB(p65), while 6-gingerol (GIN) and 6-shogaol (SHO) did not produce any significant effect. Further, we observed that the treatment with 10 µg/mL of ZOE exerted anti-inflammatory activity on LPS-stimulated young (y)HUVEC and senomorphyc activity on replicative senescent (s)HUVEC, significantly reducing the expression levels of IL-1β, TNF -α, IL-8, MCP-1, and ICAM-1. Moreover, the ZTE treatment was able to significantly reduce the IL-8 levels secreted in the medium of both LPS-stimulated yHUVEC and sHUVEC. Overall, our data suggest a potential protective role of ZOE on neuroinflammation and endothelial inflammation/activation, thus suggesting its potential relevance in delaying/postponing ARD development and progression, characterized by endothelial dysfunction. Full article
(This article belongs to the Special Issue Mechanisms of Cellular Senescence in Aging and Age-Related Diseases)
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17 pages, 5191 KiB  
Article
Critical Role of Cathepsin L/V in Regulating Endothelial Cell Senescence
by Chan Li, Zhaoya Liu, Mengshi Chen, Liyang Zhang, Ruizheng Shi and Hua Zhong
Biology 2023, 12(1), 42; https://doi.org/10.3390/biology12010042 - 26 Dec 2022
Cited by 2 | Viewed by 1783
Abstract
The senescence of vascular endothelial cells (ECs) is characterized as a hallmark of vascular aging, which leads to the initiation, progress, and advancement of cardiovascular diseases. However, the mechanism of the ECs senescence remains elusive. In this study, thoracic aortas were separated from [...] Read more.
The senescence of vascular endothelial cells (ECs) is characterized as a hallmark of vascular aging, which leads to the initiation, progress, and advancement of cardiovascular diseases. However, the mechanism of the ECs senescence remains elusive. In this study, thoracic aortas were separated from young (8-week-old) and aged (18-month-old) mice. Decreased Ctsl expression and increased vascular remodeling were observed in senescent aorta. H2O2 was used to induce human umbilical vein endothelial cells (HUVECs) senescence, as shown by increased SA-β-gal positive cells and upregulated p21 level. CTSV significantly decreased after H2O2 treatment, while over-expression of CTSV by adenovirus reduced cellular senescence. RNA sequencing analysis was conducted subsequently, and ALDH1A2 was observed to significantly increased in H2O2 group and decreased after over-expression of CTSV. This result was further confirmed by RT-PCR and WB. Moreover, over-expression of CTSV reduced the increase of ERK1/2 and AKT phosphorylation induced by H2O2. Additionally, retinoic acid (RA), the major production of ALDH1A2, was added to CTSV over-expressed senescent HUVECs. Administration of RA activated AKT and ERK1/2, induced the expression of p21, and enhanced SA-β-gal positive cells, while not affecting the expression of CTSV and ALDH1A2. These results were further confirmed in doxorubicin (DOX)-induced senescent ECs. In conclude, we have identified that Ctsl/CTSV plays a key role in ECs senescence by regulating ALDH1A2 to activate AKT/ ERK1/2-P21 pathway. Therefore, targeting Ctsl/CTSV may be a potential therapeutic strategy in EC senescence. Full article
(This article belongs to the Special Issue Mechanisms of Cellular Senescence in Aging and Age-Related Diseases)
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