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Inflammaging, Cellular Senescence and Oxidative Stress in Aging and Age-Related Disorders

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 (31 January 2021) | Viewed by 9887

Special Issue Editor

Prof. Dr. Daniela Monti

E-Mail Website1 Website2
Guest Editor
Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50134 Florence, Italy
Interests: aging and age-related diseases; longevity; centenarians and their offsprings; inflammaging; oxidative stress; genetics and epigenetics; metabolomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the normal aging process, both cumulative oxidative stress and low-grade inflammation (inflammaging) play a key role. Advanced age is associated with an increased incidence of chronic diseases, such as cardiovascular and neurodegenerative disorders, cancer and type 2 diabetes, which share oxidative stress and inflammation as pathogenetic mechanisms. It is evident that oxidative stress and inflammation share interdependent mechanisms, and can stimulate and exacerbate each other. Indeed, aging has been associated with increased production of reactive oxygen species and concomitant antioxidant system impairment, favoring the induction of cellular senescence and inflammation. Growing evidence suggests that during aging the rate of accumulation of senescent cells with a pro-inflammatory secretory phenotype (SASP) increases, which contributes to spreading inflammaging at the systemic level. This Special Issue is devoted to disentangling and understanding some of these complex mechanisms and identifying the major contributor(s) of aging and age-related diseases. In addition, multidisciplinary approaches are desirable to pinpoint new strategies to prevent/reduce the oxidative stress, cellular senescence and inflammaging able to postpone the onset of age-related pathologies and enable long-term health to the elderly.

This Special Issue will cover a selection of updated reviews and articles concerning on inflammation, cellular senescence and oxidative stress in aging process.

Prof. Dr. Daniela Monti
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

  • aging
  • age-related diseases
  • oxidative stress
  • low-grade chronic inflammation (inflammaging)
  • cellular senescence
  • anti-oxidant supplements
  • anti-inflammatory treatments
  • nutraceuticals

Related Special Issue

Published Papers (2 papers)

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Research

15 pages, 3490 KiB  
Article
Galectin-3 Modulates Macrophage Activation and Contributes Smooth Muscle Cells Apoptosis in Abdominal Aortic Aneurysm Pathogenesis
by Hsin-Ying Lu, Chun-Ming Shih, Chun-Yang Huang, Alexander T. H. Wu, Tsai-Mu Cheng, Fwu-Long Mi and Chun-Che Shih
Int. J. Mol. Sci. 2020, 21(21), 8257; https://doi.org/10.3390/ijms21218257 - 04 Nov 2020
Cited by 8 | Viewed by 3069
Abstract
Galectin-3 (Gal-3) is a 26-kDa lectin that regulates many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to abdominal aortic aneurysm (AAA) progression by enhancing monocyte chemoattraction through macrophage activation. We analyzed the plasma levels of [...] Read more.
Galectin-3 (Gal-3) is a 26-kDa lectin that regulates many aspects of inflammatory cell behavior. We assessed the hypothesis that increased levels of Gal-3 contribute to abdominal aortic aneurysm (AAA) progression by enhancing monocyte chemoattraction through macrophage activation. We analyzed the plasma levels of Gal-3 in 76 patients with AAA (AAA group) and 97 controls (CTL group) as well as in angiotensin II (Ang-II)-infused ApoE knockout mice. Additionally, conditioned media (CM) were used to polarize THP-1 monocyte to M1 macrophages with or without Gal-3 inhibition through small interfering RNA targeted deletion to investigate whether Gal-3 inhibition could attenuate macrophage-induced inflammation and smooth muscle cell (SMC) apoptosis. Our results showed a markedly increased expression of Gal-3 in the plasma and aorta in the AAA patients and experimental mice compared with the CTL group. An in vitro study demonstrated that the M1 cells exhibited increased Gal-3 expression. Gal-3 inhibition markedly decreased the quantity of macrophage-induced inflammatory regulators, including IL-8, TNF-α, and IL-1β, as well as messenger RNA expression and MMP-9 activity. Moreover, Gal-3-deficient CM weakened SMC apoptosis through Fas activation. These findings prove that Gal-3 may contribute to AAA progression by the activation of inflammatory macrophages, thereby promoting SMC apoptosis. Full article
(This article belongs to the Special Issue Inflammaging, Cellular Senescence and Oxidative Stress in Aging and Age-Related Disorders)
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23 pages, 9873 KiB  
Article
Quercetin Attenuates Pancreatic and Renal D-Galactose-Induced Aging-Related Oxidative Alterations in Rats
by Ali H. El-Far, Mohamed A. Lebda, Ahmed E. Noreldin, Mustafa S. Atta, Yaser H. A. Elewa, Mohamed Elfeky and Shaker A. Mousa
Int. J. Mol. Sci. 2020, 21(12), 4348; https://doi.org/10.3390/ijms21124348 - 18 Jun 2020
Cited by 43 | Viewed by 6291
Abstract
Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials [...] Read more.
Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials of quercetin against D-galactose (D-gal)-associated oxidative alterations that were induced experimentally in male Wistar rats. Forty-five rats were randomly allocated into five groups of nine rats each. The groups were a control group that was reared on a basal diet and injected subcutaneously with 120 mg D-gal dissolved in physiological saline solution (0.9% NaCl) per kg body weight daily and quercetin-treated groups that received the same basal diet and subcutaneous daily D-gal injections were supplemented orally with 25, 50, and 100 mg of quercetin per kg body weight for 42 days. Pancreatic and renal samples were subjected to histopathological, immunohistochemical, and relative mRNA expression assessments. Aging (p53, p21, IL-6, and IL-8), apoptotic (Bax, CASP-3, and caspase-3 protein), proliferative (Ki67 protein), antiapoptotic (Bcl2 and Bcl2 protein), inflammatory (NF-κB, IL-1β, and TNF-α), antioxidant (SOD1), and functional markers (GCLC and GCLM genes and insulin, glucagon, and podocin proteins) were determined to evaluate the oxidative alterations induced by D-gal and the protective role of quercetin. D-gal caused oxidative alterations of the pancreas and kidneys observed via upregulations of aging, apoptotic, and inflammatory markers and downregulated the antiapoptotic, proliferative, antioxidant, and functional markers. Quercetin potentially attenuated these aging-related oxidative alterations in a dose-dependent manner. Finally, we can conclude that quercetin supplementation is considered as a promising natural protective compound that could be used to delay the aging process and to maintain human health. Full article
(This article belongs to the Special Issue Inflammaging, Cellular Senescence and Oxidative Stress in Aging and Age-Related Disorders)
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