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Mechanism of Longevity
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Mechanism of Longevity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 December 2018) | Viewed by 20549

Special Issue Editor

Prof. Dr. Irmgard Tegeder

E-Mail Website
Guest Editor
Pharmazentrum Frankfurt, Dept. of Clinical Pharmacology, Goethe-University of Frankfurt, Theodor Stern Kai 7, Bd. 74, 4th Fl, 60590 Frankfurt am Main, Germany
Interests: nerve injury and neuropathic pain; pain and aging; central adaptations to chronic pain; multiple sclerosis; neuroinflammation; neuro-immunologic communication; redox signaling; nitric oxide; endocannabinoids and other lipid signaling molecules; progranulin; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging describes a time-dependent progressive decline of function with increasing age, and the hope for anti-aging strategies or medications has been motivated researchers for ages to unravel the mechanisms. More recently, “longevity”, i.e., maintenance of a long and healthy life, has been recognized as a unique feature, not simply the opposite of aging, but characterized by a positive gain of resource-sparing functions, such as change of enzyme activity, enhancement of the clearance of cellular waste, or adaptations to mild challenges, which increase the resilience towards major stressors. It is particularly intriguing to unravel how sociality and internal reward mechanisms help to extent neuronal life and circuits and hence, the individual’s life.

In the present Special Issue, we invite contributions addressing mechanisms of longevity, including all aspects from genetic, epigenetic, metabolic, endocrine, immune or redox-mediated mechanisms to environmental factors such as nutrition, sleep, social life or exercise. Original research papers and reviews are equally welcome and may involve in vitro and in vivo studies in different cells and organisms. The Special Issue will emphasize common and specific mechanisms adopted by various organisms to maintain a long and healthy life and highlight translational aspects ranging from molecules to human life at old age.

Prof. Dr. Irmgard Tegeder
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

  • longevity
  • lifespan
  • aging
  • survival
  • senescence
  • old age
  • youth

Published Papers (3 papers)

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Research

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11 pages, 1134 KiB  
Article
High Body Mass Index is Associated with Elevated Blood Levels of Progerin mRNA
by Moritz Messner, Santhosh Kumar Ghadge, Thomas Schuetz, Herbert Seiringer, Gerhard Pölzl and Marc-Michael Zaruba
Int. J. Mol. Sci. 2019, 20(8), 1976; https://doi.org/10.3390/ijms20081976 - 23 Apr 2019
Cited by 3 | Viewed by 6760
Abstract
Obesity is a well-described risk factor resulting in premature aging of the cardiovascular system ultimately limiting longevity. Premature cardiac death and aging is the hallmark of Hutchinson–Gilford syndrome (HGPS), a disease caused by defined mutations in the lamin A gene leading to a [...] Read more.
Obesity is a well-described risk factor resulting in premature aging of the cardiovascular system ultimately limiting longevity. Premature cardiac death and aging is the hallmark of Hutchinson–Gilford syndrome (HGPS), a disease caused by defined mutations in the lamin A gene leading to a shortened prelamin A protein known as progerin. Since small amounts of progerin are expressed in healthy individuals we aimed to investigate the association of Body-Mass-Index (BMI) with respect to expression of progerin mRNA in blood samples of patient with known cardiovascular disease. In this cross-sectional retrospective analysis, 111 patients were consecutively included of which 46 were normal (BMI < 25 kg/m2) and 65 overweight (BMI ≥ 25.0 kg/m2). Blood samples were analyzed for quantitative expression of progerin mRNA. Progerin as well as high-sensitive C-Reactive Protein (hs-CRP) levels were significantly upregulated in the overweight group. Linear regression analyses showed a significant positive correlation of BMI and progerin mRNA (n = 111; r = 0.265, p = 0.005), as well as for hs-CRP (n = 110; r = 0.300, p = 0.001) and for Hb1Ac (n = 110; r = 0.336, p = 0.0003). Our data suggest that BMI strongly correlates with progerin mRNA expression and inflammation. Progerin might contribute to well described accelerated biologic aging in obese individuals. Full article
(This article belongs to the Special Issue Mechanism of Longevity)
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Review

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20 pages, 1116 KiB  
Review
Approaches towards Longevity: Reprogramming, Senolysis, and Improved Mitotic Competence as Anti-Aging Therapies
by Sofia Melo Pereira, Rui Ribeiro and Elsa Logarinho
Int. J. Mol. Sci. 2019, 20(4), 938; https://doi.org/10.3390/ijms20040938 - 21 Feb 2019
Cited by 19 | Viewed by 7717
Abstract
Mainstream approaches that are currently used as anti-aging therapies primarily explore the senescence and epigenetic drift aging hallmarks and they are at two ends of the spectrum. While senolytic therapies include either the selective elimination of senescent cells or the disruption of their [...] Read more.
Mainstream approaches that are currently used as anti-aging therapies primarily explore the senescence and epigenetic drift aging hallmarks and they are at two ends of the spectrum. While senolytic therapies include either the selective elimination of senescent cells or the disruption of their secretome with the use of drugs or natural compounds, cellular reprogramming uses genetic manipulation to revert cells all the way back to pluripotency. Here, we describe the progress that has been made on these therapies, while highlighting the major challenges involved. Moreover, based on recent findings elucidating the impact of mitotic shutdown and aneuploidy in cellular senescence, we discuss the modulation of mitotic competence as an alternative strategy to delay the hallmarks of aging. We propose that a regulated rise in mitotic competence of cells could circumvent certain limitations that are present in the senolytic and reprogramming approaches, by acting to decelerate senescence and possibly restore the epigenetic landscape. Full article
(This article belongs to the Special Issue Mechanism of Longevity)
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16 pages, 1761 KiB  
Review
New Insights into the Role of Epithelial–Mesenchymal Transition during Aging
by Francisco Santos, Cristiana Moreira, Sandrina Nóbrega-Pereira and Bruno Bernardes de Jesus
Int. J. Mol. Sci. 2019, 20(4), 891; https://doi.org/10.3390/ijms20040891 - 19 Feb 2019
Cited by 34 | Viewed by 5331
Abstract
Epithelial–mesenchymal transition (EMT) is a cellular process by which differentiated epithelial cells undergo a phenotypic conversion to a mesenchymal nature. The EMT has been increasingly recognized as an essential process for tissue fibrogenesis during disease and normal aging. Higher levels of EMT proteins [...] Read more.
Epithelial–mesenchymal transition (EMT) is a cellular process by which differentiated epithelial cells undergo a phenotypic conversion to a mesenchymal nature. The EMT has been increasingly recognized as an essential process for tissue fibrogenesis during disease and normal aging. Higher levels of EMT proteins in aged tissues support the involvement of EMT as a possible cause and/or consequence of the aging process. Here, we will highlight the existing understanding of EMT supporting the phenotypical alterations that occur during normal aging or pathogenesis, covering the impact of EMT deregulation in tissue homeostasis and stem cell function. Full article
(This article belongs to the Special Issue Mechanism of Longevity)
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