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Advances in Anti-Aging Treatment Development, 2nd Edition

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: 20 December 2024 | Viewed by 5348

Special Issue Editors

Dr. Emanuele Marzetti

E-Mail Website
Guest Editor
Department of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
Interests: geriatrics; sarcopenia; frailty; geriatric syndromes; geroscience; biomarkers; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals
Dr. Anna Picca

E-Mail Website
Guest Editor
Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Roma, Italy
Interests: mitochondrial DNA; mitochondrial biogenesis; mitochondria; mitochondrial diseases; mitochondrial dynamics; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflamm-aging is the term used to refer to the chronic low-grade inflammation that develops during aging and accompanies both the development of chronic diseases (e.g., cancer, diabetes, cardiovascular disease, neurodegeneration) and functional decline in older adults. Derangements in cellular quality control systems are responsible for the accrual of intracellular “waste” (e.g., protein aggregates, damaged mitochondria, lipofuscin) and represent candidate mechanisms for the development of inflamm-aging. Indeed, many of these molecules have pro-inflammatory natures and can be released at the systemic level unless efficiently cleared. The mechanisms that regulate the displacement of these molecules are among the processes that must be tackled for the development of anti-inflammatory strategies. Additional molecular pathways that become dysregulated during aging may actively contribute to local and systemic inflammation and thus warrant investigation.

This Special Issue aims to gather contributions from researchers in the field of biogerontology and geroscience who are investigating anti-aging remedies and personalized anti-inflammatory interventions to extend one’s health- and lifespan.

We invite you to submit your latest original research or review articles to this Special Issue.

Dr. Emanuele Marzetti
Dr. Anna Picca
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

  • healthspan
  • lifespan
  • hallmarks of aging
  • cellular quality control
  • inflammation
  • gut microbiota
  • geroscience
  • intercellular signaling
  • geroprotective interventions
  • chronic conditions

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Related Special Issue

Published Papers (3 papers)

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Research

19 pages, 5005 KiB  
Article
Inhibiting miR–618 Promotes Keratinocytes Proliferation and Migration to Enhance Wound Healing in Mice
by Lingling Wu, Wenjun Fu, Yiyang Cao, Shuo Zhao, Yuchen Zhang, Xiaonan Li, Naijun Dong, Wenxin Qi, Rabia Malik, Jiao Wang and Robert Chunhua Zhao
Int. J. Mol. Sci. 2024, 25(14), 7617; https://doi.org/10.3390/ijms25147617 - 11 Jul 2024
Viewed by 1032
Abstract
The delay in wound healing caused by chronic wounds or pathological scars is a pressing issue in clinical practice, imposing significant economic and psychological burdens on patients. In particular, with the aging of the population and the increasing incidence of diseases such as [...] Read more.
The delay in wound healing caused by chronic wounds or pathological scars is a pressing issue in clinical practice, imposing significant economic and psychological burdens on patients. In particular, with the aging of the population and the increasing incidence of diseases such as diabetes, impaired wound healing is one of the growing health problems. MicroRNA (miRNA) plays a crucial role in wound healing and regulates various biological processes. Our results show that miR–618 was significantly upregulated during the inflammatory phase of wound healing.Subsequently, miR–618 promotes the secretion of pro–inflammatory cytokines and regulates the proliferation and migration of keratinocytes. Mechanistically, miR–618 binds to the target gene–Atp11b and inhibits the PI3K–Akt signaling pathway, inhibiting the epithelial–mesenchymal transition (EMT) of keratinocytes. In addition, the PI3K–Akt signaling pathway induces the enrichment of nuclear miR–618, and miR–618 binds to the promoter of Lin7a to regulate gene transcription. Intradermal injection of miR–618 antagomir around full–thickness wounds in peridermal mice effectively accelerates wound closure compared to control. In conclusion, miR–618 antagomir can be a potential therapeutic agent for wound healing. Full article
(This article belongs to the Special Issue Advances in Anti-Aging Treatment Development, 2nd Edition)
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14 pages, 3447 KiB  
Article
Addition of Polyphenols to Drugs: The Potential of Controlling “Inflammaging” and Fibrosis in Human Senescent Lung Fibroblasts In Vitro
by Maria Carolina Ximenes de Godoy, Gabriela Arruda Monteiro, Bárbara Hakim de Moraes, Juliana Alves Macedo, Gisele Mara Silva Gonçalves and Alessandra Gambero
Int. J. Mol. Sci. 2024, 25(13), 7163; https://doi.org/10.3390/ijms25137163 - 28 Jun 2024
Cited by 2 | Viewed by 1660
Abstract
The combination of a polyphenol, quercetin, with dasatinib initiated clinical trials to evaluate the safety and efficacy of senolytics in idiopathic pulmonary fibrosis, a lung disease associated with the presence of senescent cells. Another approach to senotherapeutics consists of controlling inflammation related to [...] Read more.
The combination of a polyphenol, quercetin, with dasatinib initiated clinical trials to evaluate the safety and efficacy of senolytics in idiopathic pulmonary fibrosis, a lung disease associated with the presence of senescent cells. Another approach to senotherapeutics consists of controlling inflammation related to cellular senescence or “inflammaging”, which participates, among other processes, in establishing pulmonary fibrosis. We evaluate whether polyphenols such as caffeic acid, chlorogenic acid, epicatechin, gallic acid, quercetin, or resveratrol combined with different senotherapeutics such as metformin or rapamycin, and antifibrotic drugs such as nintedanib or pirfenidone, could present beneficial actions in an in vitro model of senescent MRC-5 lung fibroblasts. A senescent-associated secretory phenotype (SASP) was evaluated by the measurement of interleukin (IL)-6, IL-8, and IL-1β. The senescent-associated β-galactosidase (SA-β-gal) activity and cellular proliferation were assessed. Fibrosis was evaluated using a Picrosirius red assay and the gene expression of fibrosis-related genes. Epithelial-mesenchymal transition (EMT) was assayed in the A549 cell line exposed to Transforming Growth Factor (TGF)-β in vitro. The combination that demonstrated the best results was metformin and caffeic acid, by inhibiting IL-6 and IL-8 in senescent MRC-5 cells. Metformin and caffeic acid also restore cellular proliferation and reduce SA-β-gal activity during senescence induction. The collagen production by senescent MRC-5 cells was inhibited by epicatechin alone or combined with drugs. Epicatechin and nintedanib were able to control EMT in A549 cells. In conclusion, caffeic acid and epicatechin can potentially increase the effectiveness of senotherapeutic drugs in controlling lung diseases whose pathophysiological component is the presence of senescent cells and fibrosis. Full article
(This article belongs to the Special Issue Advances in Anti-Aging Treatment Development, 2nd Edition)
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12 pages, 1979 KiB  
Article
Cistanche deserticola Polysaccharide Reduces Inflammation and Aging Phenotypes in the Dermal Fibroblasts through the Activation of the NRF2/HO-1 Pathway
by Kento Takaya, Toru Asou and Kazuo Kishi
Int. J. Mol. Sci. 2023, 24(21), 15704; https://doi.org/10.3390/ijms242115704 - 28 Oct 2023
Cited by 6 | Viewed by 1760
Abstract
Dermal fibroblasts maintain the skin homeostasis by interacting with the epidermis and extracellular matrix. Their senescence contributes to functional defects in the skin related to aging. Therefore, there is an urgent need for novel therapeutic agents that could inhibit fibroblast senescence. In this [...] Read more.
Dermal fibroblasts maintain the skin homeostasis by interacting with the epidermis and extracellular matrix. Their senescence contributes to functional defects in the skin related to aging. Therefore, there is an urgent need for novel therapeutic agents that could inhibit fibroblast senescence. In this study, we investigated the effects of Cistanche deserticola polysaccharide (CDP), a natural anti-inflammatory component, on the progression of senescence in human dermal fibroblasts. Normal human dermal fibroblasts (NHDFs) were cultured in passages, and highly senescent cells were selected as senescent cells. CDP treatment increased the cell proliferation in senescent NHDFs and decreased the proportion of senescence-associated-β-galactosidase-positive cells. The treatment suppressed the senescence-related secretory phenotype, and reactive oxygen species (ROS) production was reduced, alleviating H2O2-induced oxidative stress. CDP mitigated ROS formation via the nuclear factor erythroid 2-related factor/heme oxygenase-1 pathway in senescent cells and was involved in the suppression of upstream p-extracellular signal-regulated kinase. These results indicate that CDP is an antioxidant that can alleviate age-related inflammation and may be a useful compound for skin anti-aging. Full article
(This article belongs to the Special Issue Advances in Anti-Aging Treatment Development, 2nd Edition)
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