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Biomolecules
Special Issues
Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies
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Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 16611

Special Issue Editors

Prof. Dr. Undurti N. Das

E-Mail Website
Guest Editor
1. UND Life Sciences, 2221 NW 5th St, Battle Ground, WA 98604, USA
2. Department of Medicine, Omega Hospitals, Gachibowli, Hyderabad-500032, India
3. Department of Biotechnology, Indian Institute of Technology, Sangareddy 502284, India
Interests: bioactive lipids; essential fatty acids; polyunsaturated fatty acids; prostaglandins; lipoxins; resolvins; protectins and maresins; reactive oxygen species; lipid peroxidation; cancer; rheumatology; inflammation; immune response; immune checkpoint inhibitors; lupus; radiation induced injury; diabetes mellitus; insulin resistance
Special Issues, Collections and Topics in MDPI journals
Dr. Abhirup Das

E-Mail Website
Guest Editor
St. George and Sutherland Clinical School, University of New South Wales, Sydney, Australia
Interests: aging; neurodegenerative diseases; immunometabolism

Special Issue Information

Dear Colleagues,

With the increasing age of the population throughout the world, aging-associated diseases are becoming common. Some of these diseases/disorders include obesity, insulin resistance, type 2 diabetes mellitus, hypertension, metabolic syndrome, coronary heart disease, chronic obstructive lung disease (COPD), gastrointestinal disorders such as lack of appetite, inflammatory bowel disease, and constipation, hepatic disorders (due to alcoholism and previous viral diseases such as HBV and HCV), Alzheimer’s disease, depression, dementia, sarcopenia, osteoporosis, immunodeficiency, autoimmune disorders, and cancer. It is known that some of these diseases do occur in the young, but, when they occur in the elderly, they are more difficult to manage due to other associated health issues, such as diabetes mellitus, obesity, osteoporosis, and immunodeficiency. Aging is also associated with reduced wound healing, atherosclerosis, peripheral vascular disease, and decreased ability to fight infections. As the population is aging and with many elderly people actively working, it is essential that the elderly remain healthy, active, and contribute to the economy. In view of this, understanding the pathobiology of aging-associated diseases/disorders is important for the development of newer therapeutic interventions.

In this Special Issue devoted to age-related diseases, we are expecting contributions from scientists, physicians, and others on all aspects of aging. We are particularly interested in receiving manuscripts that describe the molecular events that occur in various age-related diseases/disorders and their potential therapeutic applications. Thus, we wish to bridge the gap between the lab and the clinic and, at the same time, understand the molecular events in various diseases that may also have relevance when those diseases occur in the younger population.

Prof. Dr. Undurti N. Das
Dr. Abhirup Das
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. Biomolecules 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

  • aging
  • inflammation
  • cytokines
  • resolution
  • homeostasis
  • diabetes mellitus
  • hypertension
  • diseases
  • disorders

Published Papers (5 papers)

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Research

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11 pages, 4223 KiB  
Communication
Attenuation of the Counter-Regulatory Glucose Response in CVLM C1 Neurons: A Possible Explanation for Anorexia of Aging
by Hajira Ramlan and Hanafi Ahmad Damanhuri
Biomolecules 2022, 12(3), 449; https://doi.org/10.3390/biom12030449 - 14 Mar 2022
Cited by 1 | Viewed by 1713
Abstract
This study aimed to determine the effect of age on CVLM C1 neuron glucoregulatory proteins in the feeding pathway. Male Sprague Dawley rats aged 3 months and 24 months old were divided into two subgroups: the treatment group with 2-deoxy-d-glucose (2DG) [...] Read more.
This study aimed to determine the effect of age on CVLM C1 neuron glucoregulatory proteins in the feeding pathway. Male Sprague Dawley rats aged 3 months and 24 months old were divided into two subgroups: the treatment group with 2-deoxy-d-glucose (2DG) and the control group. Rat brains were dissected to obtain the CVLM region of the brainstem. Western blot was used to determine protein expression of tyrosine hydroxylase (TH), phosphorylated TH at Serine40 (pSer40TH), AMP-activated protein kinase (AMPK), phosphorylated AMPK (phospho AMPK), and neuropeptide Y Y5 receptors (NPY5R) in CVLM samples. Immunofluorescence was used to determine TH-, AMPK-, and NPY5R-like immunoreactivities among other brain coronal sections. Results obtained denote a decrease in basal TH phosphorylation levels and AMPK proteins and an increase in TH proteins among aged CVLM neurons. Increases in the basal immunoreactivity of TH+, AMPK+, NPY5R+, TH+/AMPK+, and TH+/NPY5R+ were also observed among old rats. Young treatment-group rats saw a decrease in TH phosphorylation and AMPK proteins following 2DG administration, while an increase in AMPK phosphorylation and a decrease in TH proteins were found among the old-treatment-group rats. These findings suggest the participation of CVLM C1 neurons in counter-regulatory responses among young and old rats. Altering protein changes in aged CVLM C1 neurons may attenuate responses to glucoprivation, thus explaining the decline in food intake among the elderly. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies)
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22 pages, 2351 KiB  
Article
Prognostic Signature of Chronic Kidney Disease in Advanced Age: Secondary Analysis from the InGAH Study with One-Year Follow-Up
by Anna Maria Meyer, Lena Pickert, Annika Heeß, Ingrid Becker, Christine Kurschat, Malte P. Bartram, Thomas Benzing and Maria Cristina Polidori
Biomolecules 2022, 12(3), 423; https://doi.org/10.3390/biom12030423 - 09 Mar 2022
Cited by 1 | Viewed by 2394
Abstract
The negative impact of chronic kidney disease (CKD) on health status and quality of life in older patients has been well documented. However, data on frailty trajectories and long-term outcomes of older CKD patients undergoing structured Comprehensive Geriatric Assessment (CGA) with multidimensional frailty [...] Read more.
The negative impact of chronic kidney disease (CKD) on health status and quality of life in older patients has been well documented. However, data on frailty trajectories and long-term outcomes of older CKD patients undergoing structured Comprehensive Geriatric Assessment (CGA) with multidimensional frailty evaluation are sparse. Here, we analysed records from 375 CKD patients admitted to our university hospital (mean age 77.5 (SD 6.1) years, 36% female) who had undergone a CGA-based calculation of the frailty score with the multidimensional prognostic index (MPI) as well as follow-up evaluations at 3, 6 and 12 months after discharge. Based on the MPI score at admission, 21% of the patients were frail and 56% were prefrail. MPI values were significantly associated with KDIGO CKD stages (p = 0.003) and rehospitalisation after 6 months (p = 0.027) and mortality at 3, 6 and 12 months (p = 0.001), independent of chronological age. Kidney transplant recipients (KTR) showed a significantly lower frailty compared to patients with renal replacement therapy (RRT, p = 0.028). The association between frailty and mortality after 12 months appeared particularly strong for KTR (mean MPI 0.43 KTR vs. 0.52 RRT, p < 0.001) and for patients with hypoalbuminemia (p < 0.001). Interestingly, RRT was per se not significantly associated with mortality during follow up. However, compared to patients on RRT those with KTR had a significantly lower grade of care (p = 0.031) and lower rehospitalisation rates at 12 months (p = 0.010). The present analysis shows that the large majority of older CKD inpatients are prefrail or frail and that the risk for CKD-related adverse outcomes on the long term can be accurately stratified by CGA-based instruments. Further studies are needed to explore the prognostic and frailty-related signature of laboratory biomarkers in CKD. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies)
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16 pages, 1759 KiB  
Article
Characterization of Stress Responses in a Drosophila Model of Werner Syndrome
by Derek G. Epiney, Charlotte Salameh, Deirdre Cassidy, Luhan T. Zhou, Joshua Kruithof, Rolan Milutinović, Tomas S. Andreani, Aaron E. Schirmer and Elyse Bolterstein
Biomolecules 2021, 11(12), 1868; https://doi.org/10.3390/biom11121868 - 12 Dec 2021
Cited by 4 | Viewed by 3099
Abstract
As organisms age, their resistance to stress decreases while their risk of disease increases. This can be shown in patients with Werner syndrome (WS), which is a genetic disease characterized by accelerated aging along with increased risk of cancer and metabolic disease. WS [...] Read more.
As organisms age, their resistance to stress decreases while their risk of disease increases. This can be shown in patients with Werner syndrome (WS), which is a genetic disease characterized by accelerated aging along with increased risk of cancer and metabolic disease. WS is caused by mutations in WRN, a gene involved in DNA replication and repair. Recent research has shown that WRN mutations contribute to multiple hallmarks of aging including genomic instability, telomere attrition, and mitochondrial dysfunction. However, questions remain regarding the onset and effect of stress on early aging. We used a fly model of WS (WRNexoΔ) to investigate stress response during different life stages and found that stress sensitivity varies according to age and stressor. While larvae and young WRNexoΔ adults are not sensitive to exogenous oxidative stress, high antioxidant activity suggests high levels of endogenous oxidative stress. WRNexoΔ adults are sensitive to stress caused by elevated temperature and starvation suggesting abnormalities in energy storage and a possible link to metabolic dysfunction in WS patients. We also observed higher levels of sleep in aged WRNexoΔ adults suggesting an additional adaptive mechanism to protect against age-related stress. We suggest that stress response in WRNexoΔ is multifaceted and evokes a systemic physiological response to protect against cellular damage. These data further validate WRNexoΔ flies as a WS model with which to study mechanisms of early aging and provide a foundation for development of treatments for WS and similar diseases. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies)
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13 pages, 453 KiB  
Article
Gut-Derived Endotoxin and Telomere Length Attrition in Adults with and without Type 2 Diabetes
by Nasser M. Al-Daghri, Saba Abdi, Shaun Sabico, Abdullah M. Alnaami, Kaiser A. Wani, Mohammed G. A. Ansari, Malak Nawaz Khan Khattak, Nasiruddin Khan, Gyanendra Tripathi, George P. Chrousos and Philip G. McTernan
Biomolecules 2021, 11(11), 1693; https://doi.org/10.3390/biom11111693 - 14 Nov 2021
Cited by 8 | Viewed by 2640
Abstract
Premature aging, as denoted by a reduced telomere length (TL), has been observed in several chronic inflammatory diseases, such as obesity and type 2 diabetes mellitus (T2DM). However, no study to date has addressed the potential inflammatory influence of the gut-derived Gram-negative bacterial [...] Read more.
Premature aging, as denoted by a reduced telomere length (TL), has been observed in several chronic inflammatory diseases, such as obesity and type 2 diabetes mellitus (T2DM). However, no study to date has addressed the potential inflammatory influence of the gut-derived Gram-negative bacterial fragments lipopolysaccharide, also referred to as endotoxin, and its influence on TL in low-grade inflammatory states such as type 2 diabetes mellitus (T2DM). The current study therefore investigated the influence of endotoxin and inflammatory factors on telomere length (TL) in adults with (T2DM: n = 387) and without (non-diabetic (ND) controls: n = 417) obesity and T2DM. Anthropometric characteristics were taken, and fasted blood samples were used to measure biomarkers, TL, and endotoxin. The findings from this study highlighted across all participants that circulating endotoxin (r = −0.17, p = 0.01) was inversely associated with TL, noting that endotoxin and triglycerides predicted 18% of the variance perceived in TL (p < 0.001). Further stratification of the participants according to T2DM status and sex highlighted that endotoxin significantly predicted 19% of the variance denoted in TL among male T2DM participants (p = 0.007), where TL was notably influenced. The influence on TL was not observed to be impacted by anti-T2DM medications, statins, or anti-hypertensive therapies. Taken together, these results show that TL attrition was inversely associated with circulating endotoxin levels independent of the presence of T2DM and other cardiometabolic factors, suggesting that low-grade chronic inflammation may trigger premature biological aging. The findings further highlight the clinical relevance of mitigating the levels of circulating endotoxin (e.g., manipulation of gut microbiome) not only for the prevention of chronic diseases but also to promote healthy aging. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies)
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Review

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19 pages, 2036 KiB  
Review
The Role of Polymorphisms in Collagen-Encoding Genes in Intervertebral Disc Degeneration
by Vera V. Trefilova, Natalia A. Shnayder, Marina M. Petrova, Daria S. Kaskaeva, Olga V. Tutynina, Kirill V. Petrov, Tatiana E. Popova, Olga V. Balberova, German V. Medvedev and Regina F. Nasyrova
Biomolecules 2021, 11(9), 1279; https://doi.org/10.3390/biom11091279 - 26 Aug 2021
Cited by 22 | Viewed by 5035
Abstract
(1) Background: The purpose of this review is to analyze domestic and foreign studies on the role of collagen-encoding genes polymorphism in the development of intervertebral discs (IVDs) degeneration in humans. (2) Methods: We have carried out a search for full-text articles published [...] Read more.
(1) Background: The purpose of this review is to analyze domestic and foreign studies on the role of collagen-encoding genes polymorphism in the development of intervertebral discs (IVDs) degeneration in humans. (2) Methods: We have carried out a search for full-text articles published in e-Library, PubMed, Oxford Press, Clinical Case, Springer, Elsevier and Google Scholar databases. The search was carried out using keywords and their combinations. The search depth was 5 years (2016–2021). In addition, this review includes articles of historical interest. Despite an extensive search, it is possible that we might have missed some studies published in recent years. (3) Results: According to the data of genome-wide and associative genetic studies, the following candidate genes that play a role in the biology of IVDs and the genetic basis of the processes of collagen degeneration of the annulus fibrosus and nucleus pulposus of IVDs in humans are of the greatest interest to researchers: COL1A1, COL2A1, COL9A2, COL9A3, COL11A1 and COL11A2. In addition, the role of genes COL1A2, COL9A1 and others is being actively studied. (4) Conclusions: In our review, we summarized and systematized the available information on the role of genetic factors in IVD collagen fibers turnover and also focused on the functions of different types of collagen present in the IVD. Understanding the etiology of impaired collagen formation can allow doctors to prescribe pathogenetically-based treatment, achieving the most effective results. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies)
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