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Aging and Senescence 3.0
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Aging and Senescence 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 11783

Special Issue Editors

Prof. Dr. Giovanni Di Bernardo

E-Mail Website
Guest Editor
Department of Experimental Medicine, Luigi Vanvitelli Campania University, 80138 Naples, Italy
Interests: senescence; mesenchymal stromal cells; cell cycle; adipogenesis; apoptosis; differentiation; aging
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Umberto Galderisi

E-Mail Website
Guest Editor
Department of Experimental Medicine, Luigi Vanvitelli Campania University, 80138 Naples, Italy
Interests: stem cell; MUSE cells; cellular biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is a natural process that occurs during the lifespan of an organism and involves cellular, physiological, and social changes. Cellular senescence refers to a phenomenon in which permanent cell growth arrest is induced, for example, as a response to excessive extracellular or intracellular stress. The involved cells change and acquire a new phenotype that, by and large, defines the senescence status. Senescent cells secrete senescence-associated secretory phenotype (SASP) proteins to carry out several functions, such as sensitizing surrounding cells to senescence, immunomodulation, and impairing or fostering cancer growth and wound healing, promoting tissue remodeling. Recent studies are increasingly revealing that this event is involved in aging and age-associate diseases, considering that tissue regeneration and DNA damage repair decline with age. Nevertheless, the mechanisms and effectors that drive a gradual decay of physiological function still remain under-investigated. In this context, a recent debate in the scientific community is questioning whether aging is an adaptive action or simply a consequence of the stochastic accumulation of deleterious phenomena. The primary aspect of this Special Issue is to supply a contribution of significant works in the field of “Aging and Senescence”, focusing on biological processes of cellular senescence and the demonstration that this physiological mechanism contributes to the onset of multiple diseases associated with aging.

Topics of this Special Issue include, but are not limited to:

  • Organismal aging and senescence
  • The key role of cellular senescence in driving of aging
  • Senescence-associated secretory phenotype (SASP) proteins and their contribution to physiological and pathological effects in organisms
  • How genetic or pharmacological removal of senescent cells improves longevity and promotes a long health span
  • Stem cells and aging

Prof. Dr. Giovanni Di Bernardo
Prof. Dr. Umberto Galderisi
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. 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

  • aging
  • inflammaging
  • replicative senescence
  • replicative senescence
  • senescence-associated secretory phenotype (SASP)
  • age-associated diseases

Published Papers (5 papers)

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Research

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25 pages, 3319 KiB  
Article
Palbociclib-Induced Cellular Senescence Is Modulated by the mTOR Complex 1 and Autophagy
by Angel Cayo, Whitney Venturini, Danitza Rebolledo-Mira, Rodrigo Moore-Carrasco, Andrés A. Herrada, Estefanía Nova-Lamperti, Claudio Valenzuela and Nelson E. Brown
Int. J. Mol. Sci. 2023, 24(11), 9284; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24119284 - 26 May 2023
Cited by 1 | Viewed by 1855
Abstract
Despite not dividing, senescent cells acquire the ability to synthesize and secrete a plethora of bioactive molecules, a feature known as the senescence-associated secretory phenotype (SASP). In addition, senescent cells often upregulate autophagy, a catalytic process that improves cell viability in stress-challenged cells. [...] Read more.
Despite not dividing, senescent cells acquire the ability to synthesize and secrete a plethora of bioactive molecules, a feature known as the senescence-associated secretory phenotype (SASP). In addition, senescent cells often upregulate autophagy, a catalytic process that improves cell viability in stress-challenged cells. Notably, this “senescence-related autophagy” can provide free amino acids for the activation of mTORC1 and the synthesis of SASP components. However, little is known about the functional status of mTORC1 in models of senescence induced by CDK4/6 inhibitors (e.g., Palbociclib), or the effects that the inhibition of mTORC1 or the combined inhibition of mTORC1 and autophagy have on senescence and the SASP. Herein, we examined the effects of mTORC1 inhibition, with or without concomitant autophagy inhibition, on Palbociclib-driven senescent AGS and MCF-7 cells. We also assessed the pro-tumorigenic effects of conditioned media from Palbociclib-driven senescent cells with the inhibition of mTORC1, or with the combined inhibition of mTORC1 and autophagy. We found that Palbociclib-driven senescent cells display a partially reduced activity of mTORC1 accompanied by increased levels of autophagy. Interestingly, further mTORC1 inhibition exacerbated the senescent phenotype, a phenomenon that was reversed upon autophagy inhibition. Finally, the SASP varied upon inhibiting mTORC1, or upon the combined inhibition of mTORC1 and autophagy, generating diverse responses in cell proliferation, invasion, and migration of non-senescent tumorigenic cells. Overall, variations in the SASP of Palbociclib-driven senescent cells with the concomitant inhibition of mTORC1 seem to depend on autophagy. Full article
(This article belongs to the Special Issue Aging and Senescence 3.0)
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13 pages, 2725 KiB  
Article
Efficacy and Safety of Epidermidibacterium Keratini EPI-7 Derived Postbiotics in Skin Aging: A Prospective Clinical Study
by Jihee Kim, Young In Lee, Seyoung Mun, Jinuk Jeong, Dong-Geol Lee, Misun Kim, HyungWoo Jo, Sieun Lee, Kyudong Han and Ju Hee Lee
Int. J. Mol. Sci. 2023, 24(5), 4634; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054634 - 27 Feb 2023
Cited by 5 | Viewed by 2511
Abstract
The present study investigated the effect of topical application of Epidermidibacterium Keratini (EPI-7) ferment filtrate, which is a postbiotic product of a novel actinobacteria, on skin aging, by performing a prospective randomized split-face clinical study on Asian woman participants. The investigators measured skin [...] Read more.
The present study investigated the effect of topical application of Epidermidibacterium Keratini (EPI-7) ferment filtrate, which is a postbiotic product of a novel actinobacteria, on skin aging, by performing a prospective randomized split-face clinical study on Asian woman participants. The investigators measured skin biophysical parameters, including skin barrier function, elasticity, and dermal density, and revealed that the application of the EPI-7 ferment filtrate-including test product resulted in significantly higher improvements in barrier function, skin elasticity, and dermal density compared to the placebo group. This study also investigated the influence of EPI-7 ferment filtrate on skin microbiome diversity to access its potential beneficial effects and safety. EPI-7 ferment filtrate increased the abundance of commensal microbes belonging to Cutibacterium, Staphylococcus, Corynebacterium, Streptococcus, Lawsonella, Clostridium, Rothia, Lactobacillus, and Prevotella. The abundance of Cutibacterium was significantly increased along with significant changes in Clostridium and Prevotella abundance. Therefore, EPI-7 postbiotics, which contain the metabolite called orotic acid, ameliorate the skin microbiota linked with the aging phenotype of the skin. This study provides preliminary evidence that postbiotic therapy may affect the signs of skin aging and microbial diversity. To confirm the positive effect of EPI-7 postbiotics and microbial interaction, additional clinical investigations and functional analyses are required. Full article
(This article belongs to the Special Issue Aging and Senescence 3.0)
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17 pages, 5154 KiB  
Article
Involvement of lncRNA TUG1 in HIV-1 Tat-Induced Astrocyte Senescence
by Prakash P. Pillai, Muthukumar Kannan, Susmita Sil, Seema Singh, Annadurai Thangaraj, Ernest T. Chivero, Raghubendra Singh Dagur, Ashutosh Tripathi, Guoku Hu, Palsamy Periyasamy and Shilpa Buch
Int. J. Mol. Sci. 2023, 24(5), 4330; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054330 - 22 Feb 2023
Cited by 5 | Viewed by 2084
Abstract
HIV-1 infection in the era of combined antiretroviral therapy has been associated with premature aging. Among the various features of HIV-1 associated neurocognitive disorders, astrocyte senescence has been surmised as a potential cause contributing to HIV-1-induced brain aging and neurocognitive impairments. Recently, lncRNAs [...] Read more.
HIV-1 infection in the era of combined antiretroviral therapy has been associated with premature aging. Among the various features of HIV-1 associated neurocognitive disorders, astrocyte senescence has been surmised as a potential cause contributing to HIV-1-induced brain aging and neurocognitive impairments. Recently, lncRNAs have also been implicated to play essential roles in the onset of cellular senescence. Herein, using human primary astrocytes (HPAs), we investigated the role of lncRNA TUG1 in HIV-1 Tat-mediated onset of astrocyte senescence. We found that HPAs exposed to HIV-1 Tat resulted in significant upregulation of lncRNA TUG1 expression that was accompanied by elevated expression of p16 and p21, respectively. Additionally, HIV-1 Tat-exposed HPAs demonstrated increased expression of senescence-associated (SA) markers—SA-β-galactosidase (SA-β-gal) activity and SA-heterochromatin foci—cell-cycle arrest, and increased production of reactive oxygen species and proinflammatory cytokines. Intriguingly, gene silencing of lncRNA TUG1 in HPAs also reversed HIV-1 Tat-induced upregulation of p21, p16, SA-β gal activity, cellular activation, and proinflammatory cytokines. Furthermore, increased expression of astrocytic p16 and p21, lncRNA TUG1, and proinflammatory cytokines were observed in the prefrontal cortices of HIV-1 transgenic rats, thereby suggesting the occurrence of senescence activation in vivo. Overall, our data indicate that HIV-1 Tat-induced astrocyte senescence involves the lncRNA TUG1 and could serve as a potential therapeutic target for dampening accelerated aging associated with HIV-1/HIV-1 proteins. Full article
(This article belongs to the Special Issue Aging and Senescence 3.0)
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14 pages, 3705 KiB  
Article
Therapeutic Ultrasound Halts Progression of Chronic Kidney Disease In Vivo via the Regulation of Markers Associated with Renal Epithelial–Mesenchymal Transition and Senescence
by Chen-Yu Lin, Ching-Chia Wang, Jui-Zhi Loh, Tsai-Chen Chiang, Te-I Weng, Ding-Cheng Chan, Kuan-Yu Hung, Chih-Kang Chiang and Shing-Hwa Liu
Int. J. Mol. Sci. 2022, 23(21), 13387; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232113387 - 02 Nov 2022
Cited by 4 | Viewed by 1686
Abstract
Low-intensity pulsed ultrasound (LIPUS), a therapeutic type of ultrasound, is known to enhance bone fracture repair processes and help some tissues to heal. Here, we investigated the therapeutic potential of LIPUS for the treatment of chronic kidney disease (CKD) in two CKD mouse [...] Read more.
Low-intensity pulsed ultrasound (LIPUS), a therapeutic type of ultrasound, is known to enhance bone fracture repair processes and help some tissues to heal. Here, we investigated the therapeutic potential of LIPUS for the treatment of chronic kidney disease (CKD) in two CKD mouse models. CKD mice were induced using both unilateral renal ischemia/reperfusion injury (IRI) with nephrectomy and adenine administration. The left kidneys of the CKD mice were treated using LIPUS with the parameters of 3 MHz, 100 mW/cm2, and 20 min/day, based on the preliminary experiments. The mice were euthanized 14 days after IRI or 28 days after the end of adenine administration. LIPUS treatment effectively alleviated the decreases in the body weight and albumin/globulin ratio and the increases in the serum renal functional markers, fibroblast growth factor-23, renal pathological changes, and renal fibrosis in the CKD mice. The parameters for epithelial–mesenchymal transition (EMT), senescence-related signal induction, and the inhibition of α-Klotho and endogenous antioxidant enzyme protein expression in the kidneys of the CKD mice were also significantly alleviated by LIPUS. These results suggest that LIPUS treatment reduces CKD progression through the inhibition of EMT and senescence-related signals. The application of LIPUS may be an alternative non-invasive therapeutic intervention for CKD therapy. Full article
(This article belongs to the Special Issue Aging and Senescence 3.0)
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Review

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16 pages, 1398 KiB  
Review
The Antiaging Activities of Phytochemicals in Dark-Colored Plant Foods: Involvement of the Autophagy- and Apoptosis-Associated Pathways
by Mengliu Luo, Meiqing Mai, Wanhan Song, Qianhua Yuan, Xiaoling Feng, Enqin Xia and Honghui Guo
Int. J. Mol. Sci. 2022, 23(19), 11038; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911038 - 20 Sep 2022
Cited by 1 | Viewed by 2795
Abstract
In the last two decades, human life expectancy has increased by about 10 years, but this has not been accompanied by a corresponding increase in healthy lifespan. Aging is associated with a wide range of human disorders, including cancer, diabetes, and cardiovascular and [...] Read more.
In the last two decades, human life expectancy has increased by about 10 years, but this has not been accompanied by a corresponding increase in healthy lifespan. Aging is associated with a wide range of human disorders, including cancer, diabetes, and cardiovascular and neurodegenerative diseases. Delaying the aging of organs or tissues and improving the physiological functions of the elderly can reduce the risk of aging-related diseases. Autophagy and apoptosis are crucial mechanisms for cell survival and tissue homeostasis, and may also be primary aging-regulatory pathways. Recent epidemiological studies have shown that eating more colorful plant foods could increase life expectancy. Several representative phytochemicals in dark-colored plant foods such as quercetin, catechin, curcumin, anthocyanins, and lycopene have apparent antiaging potential. Nevertheless, the antiaging signaling pathways of the phytochemicals from dark-colored plant foods remain elusive. In the present review, we summarized autophagy- and apoptosis-associated targeting pathways of those phytochemicals and discussed the core targets involved in the antiaging effects. Further clinical evaluation and exploitation of phytochemicals as antiaging agents are needed to develop novel antiaging therapeutics for preventing age-related diseases and improving a healthy lifespan. Full article
(This article belongs to the Special Issue Aging and Senescence 3.0)
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