scholarly journals Potential of nanoparticles and nanopolymers in treatment of age-associated diseases

2021 ◽  
Vol 12 (4) ◽  
pp. 045008
Author(s):  
Fatemeh Saadatpour ◽  
Fatemeh Mohammadipanah ◽  
Nazanin Zohourian ◽  
Mahshid Hodjat
Keyword(s):  
Aging Process ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Tissue Levels ◽  
Associated Diseases ◽  
Age Related ◽  
Different Sources

Abstract Aging is an inevitable process caused by the accumulation of degenerative destructions, which ultimately leads to organism death. As the aging process occurs at the molecular, cellular, and tissue levels, understanding the whole details of age-related disorders is the prerequisite for the development of anti-aging therapy. More than 300 compounds of different sources have been reported with an anti-aging activity that controls age-related diseases through regulating single or multiple signalling pathways. Recent innovations in nanotechniques could lead to the development of nanomaterials having effects on age-associated malfunctions or acting as nanocarrier systems and distributers of anti-aging drugs. In this review, we summarised the molecular mechanisms of longevity and the prospect of developing anti-aging nanomaterials targeting aging pathways.

scholarly journals Potential of nanoparticles and nanopolymers in treatment of age-associated diseases

2021 ◽  
Author(s):  
Fatemeh Saadatpour ◽  
Fatemeh Mohammadipanah ◽  
Nazanin Zohourian ◽  
Mahshid Hodjat
Keyword(s):  
Signaling Pathways ◽  
Aging Process ◽  
Molecular Mechanisms ◽  
Aging Effects ◽  
Tissue Levels ◽  
Associated Diseases ◽  
Multiple Signaling ◽  
Different Sources

Aging is an inevitable process caused by the accumulation of degenerative destructions, which ultimately leads to organism death. As the aging process occurs at the molecular, cellular, and tissue levels, understanding the whole details is the prerequisite for the development of anti-aging therapy. More than 300 compounds of different sources have been reported with the anti-aging activity that slow aging and extend lifespan through regulating single or multiple signaling pathways. Recent innovations in nanotechniques could lead to the development of nanomaterials having anti-aging effects or acting as nanocarrier systems and distributers of anti-aging drugs. In this review, we summarized the molecular mechanisms of longevity and the prospect of developing anti-aging nanomaterials targeting aging pathways.

Molecular mechanisms of life- and health-span extension: role of calorie restriction and exercise intervention

2007 ◽  
Vol 32 (5) ◽  
pp. 954-966 ◽  
Author(s):  
Christy S. Carter ◽  
Tim Hofer ◽  
Arnold Y. Seo ◽  
Christian Leeuwenburgh
Keyword(s):  
Life Span ◽  
Calorie Restriction ◽  
Aging Process ◽  
Molecular Mechanisms ◽  
Geriatric Medicine ◽  
Functional Decline ◽  
Intervention Strategies ◽  
Health Span ◽  
Structural Deterioration ◽  
Age Related

The aging process results in a gradual and progressive structural deterioration of biomolecular and cellular compartments and is associated with many pathological conditions, including cardiovascular disease, stroke, Alzheimer’s disease, osteoporosis, sarcopenia, and liver dysfunction. Concomitantly, each of these conditions is associated with progressive functional decline, loss of independence, and ultimately disability. Because disabled individuals require care in outpatient or home care settings, and in light of the social, emotional, and fiscal burden associated with caring for an ever-increasing elderly population, research in geriatric medicine has recently focused on the biological mechanisms that are involved in the progression towards functional decline and disability to better design treatment and intervention strategies. Although not completely understood, the mechanisms underlying the aging process may partly involve inflammatory processes, oxidative damage, mitochondrial dysfunction, and apoptotic tissue degeneration. These hypotheses are based on epidemiological evidence and data from animal models of aging, as well as interventional studies. Findings from these studies have identified possible strategies to decrease the incidence of age-related diseases and delay the aging process. For example, lifelong exercise is known to extend mean life-span, whereas calorie restriction (CR) increases both mean and maximum life-span in a variety of species. Optimal application of these intervention strategies in the elderly may positively affect health-related outcomes and possibly longevity. Therefore, the scope of this article is to (i) provide an interpretation of various theories of aging from a “health-span” perspective; (ii) describe interventional testing in animals (CR and exercise); and (iii) provide a translational interpretation of these data.

Potential Possibilities of Nuclear Medicine Methods in Diagnostics Age Changes of the Cardiovascular System.

2021 ◽  
Vol 66 (5) ◽  
pp. 59-65
Author(s):  
M. Vorontsova ◽  
A. Obrezan ◽  
A. Obrezan
Keyword(s):  
Aging Process ◽  
Molecular Mechanisms ◽  
The Body ◽  
Premature Aging ◽  
Diagnostic Methods ◽  
Age Changes ◽  
Medical Interventions ◽  
Defense Systems ◽  
Age Related ◽  
Daunting Task

In connection with the increase in the average age of the world's population, the problem of preventing premature aging and the treatment of age-related diseases is coming to the fore. The main direction in the implementation of this goal is to influence the key molecular mechanisms of aging in order to suppress pathological processes and activate the defense systems of the cell and the body as a whole. In order to solve this daunting task, it is necessary to have in the arsenal not only various means of intervention in the aging process, but also diagnostic methods that would allow to fully verify these processes and evaluate the effectiveness of medical interventions.

scholarly journals Insights into the Conserved Regulatory Mechanisms of Human and Yeast Aging

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 882 ◽  
Author(s):  
Rashmi Dahiya ◽  
Taj Mohammad ◽  
Mohamed F. Alajmi ◽  
Md. Tabish Rehman ◽  
Gulam Mustafa Hasan ◽  
...  
Keyword(s):  
Aging Process ◽  
Molecular Mechanisms ◽  
Model Organism ◽  
Cellular Functions ◽  
Aging Research ◽  
Yeast Saccharomyces Cerevisiae ◽  
Age Related ◽  
Evolutionarily Conserved ◽  
Yeast Aging ◽  
Key Pathways

Aging represents a significant biological process having strong associations with cancer, diabetes, and neurodegenerative and cardiovascular disorders, which leads to progressive loss of cellular functions and viability. Astonishingly, age-related disorders share several genetic and molecular mechanisms with the normal aging process. Over the last three decades, budding yeast Saccharomyces cerevisiae has emerged as a powerful yet simple model organism for aging research. Genetic approaches using yeast RLS have led to the identification of hundreds of genes impacting lifespan in higher eukaryotes. Numerous interventions to extend yeast lifespan showed an analogous outcome in multi-cellular eukaryotes like fruit flies, nematodes, rodents, and humans. We collected and analyzed a multitude of observations from published literature and provide the contribution of yeast in the understanding of aging hallmarks most applicable to humans. Here, we discuss key pathways and molecular mechanisms that underpin the evolutionarily conserved aging process and summarize the current understanding and clinical applicability of its trajectories. Gathering critical information on aging biology would pave the way for future investigation targeted at the discovery of aging interventions.

scholarly journals Molecular Age-Related Changes in the Anterior Segment of the Eye

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Luis Fernando Hernandez-Zimbron ◽  
Rosario Gulias-Cañizo ◽  
María F. Golzarri ◽  
Blanca Elizabeth Martínez-Báez ◽  
Hugo Quiroz-Mercado ◽  
...  
Keyword(s):  
Aging Process ◽  
Molecular Mechanisms ◽  
Molecular Level ◽  
Current Knowledge ◽  
Anterior Segment ◽  
Ageing Process ◽  
Degenerative Diseases ◽  
Mesh Terms ◽  
Age Related ◽  
Age Dependent

Purpose. To examine the current knowledge about the age-related processes in the anterior segment of the eye at a biological, clinical, and molecular level. Methods. We reviewed the available published literature that addresses the aging process of the anterior segment of the eye and its associated molecular and physiological events. We performed a search on PubMed, CINAHL, and Embase using the MeSH terms “eye,” “anterior segment,” and “age.” We generated searches to account for synonyms of these keywords and MESH headings as follows: (1) “Eye” AND “ageing process” OR “anterior segment ageing” and (2) “Anterior segment” AND “ageing process” OR “anterior segment” AND “molecular changes” AND “age.” Results. Among the principal causes of age-dependent alterations in the anterior segment of the eye, we found the mutation of the TGF-β gene and loss of autophagy in addition to oxidative stress, which contributes to the pathogenesis of degenerative diseases. Conclusions. In this review, we summarize the current knowledge regarding some of the molecular mechanisms related to aging in the anterior segment of the eye. We also introduce and propose potential roles of autophagy, an important mechanism responsible for maintaining homeostasis and proteostasis under stress conditions in the anterior segment during aging.

scholarly journals ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age-Related Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Pierpaola Davalli ◽  
Tijana Mitic ◽  
Andrea Caporali ◽  
Angela Lauriola ◽  
Domenico D’Arca
Keyword(s):  
Aging Process ◽  
Molecular Mechanisms ◽  
Cell Senescence ◽  
Therapeutic Interventions ◽  
Causal Connection ◽  
Oxygen Species ◽  
The Novel ◽  
Age Related ◽  
Multiple Levels ◽  
Stress Damage

The aging process worsens the human body functions at multiple levels, thus causing its gradual decrease to resist stress, damage, and disease. Besides changes in gene expression and metabolic control, the aging rate has been associated with the production of high levels of Reactive Oxygen Species (ROS) and/or Reactive Nitrosative Species (RNS). Specific increases of ROS level have been demonstrated as potentially critical for induction and maintenance of cell senescence process. Causal connection between ROS, aging, age-related pathologies, and cell senescence is studied intensely. Senescent cells have been proposed as a target for interventions to delay the aging and its related diseases or to improve the diseases treatment. Therapeutic interventions towards senescent cells might allow restoring the health and curing the diseases that share basal processes, rather than curing each disease in separate and symptomatic way. Here, we review observations on ROS ability of inducing cell senescence through novel mechanisms that underpin aging processes. Particular emphasis is addressed to the novel mechanisms of ROS involvement in epigenetic regulation of cell senescence and aging, with the aim to individuate specific pathways, which might promote healthy lifespan and improve aging.

scholarly journals Natural Compounds and Aging: Between Autophagy and Inflammasome

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Shih-Yi Chuang ◽  
Chih-Hung Lin ◽  
Jia-You Fang
Keyword(s):  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Natural Compounds ◽  
Inflammasome Activation ◽  
Defense Systems ◽  
Age Related ◽  
Nlrp3 Inflammasome Activation ◽  
The Relationship ◽  
Different Sources

Aging, a natural physiological process, is characterized by a progressive loss of physiological integrity. Loss of cellular homeostasis in the aging process results from different sources, including changes in genes, cell imbalance, and dysregulation of the host-defense systems. Innate immunity dysfunctions during aging are connected with several human pathologies, including metabolic disorders and cardiovascular diseases. Recent studies have clearly indicated that the decline in autophagic capacity that accompanies aging results in the accumulation of dysfunctional mitochondria, reactive oxygen species (ROS) production, and further process dysfunction of the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation in the macrophages, which produce the proinflammatory cytokines. These factors impair cellular housekeeping and expose cells to higher risk in many age-related diseases, such as atherosclerosis and type 2 diabetes. In this review, we investigated the relationship between dysregulation of the inflammasome activation and perturbed autophagy with aging as well as the possible molecular mechanisms. We also summarized the natural compounds from food intake, which have potential to reduce the inflammasome activation and enhance autophagy and can further improve the age-related diseases discussed in this paper.

The Role of Vascular Aging in Atherosclerotic Plaque Development and Vulnerability

2019 ◽  
Vol 25 (29) ◽  
pp. 3098-3111 ◽  
Author(s):  
Luca Liberale ◽  
Giovanni G. Camici
Keyword(s):  
Atherosclerotic Plaque ◽  
Molecular Mechanisms ◽  
Driving Forces ◽  
Plaque Burden ◽  
Vascular Aging ◽  
Age Related ◽  
Plaque Development ◽  
Increased Risk ◽  
The Impact ◽  
Over Time

Background: The ongoing demographical shift is leading to an unprecedented aging of the population. As a consequence, the prevalence of age-related diseases, such as atherosclerosis and its thrombotic complications is set to increase in the near future. Endothelial dysfunction and vascular stiffening characterize arterial aging and set the stage for the development of cardiovascular diseases. Atherosclerotic plaques evolve over time, the extent to which these changes might affect their stability and predispose to sudden complications remains to be determined. Recent advances in imaging technology will allow for longitudinal prospective studies following the progression of plaque burden aimed at better characterizing changes over time associated with plaque stability or rupture. Oxidative stress and inflammation, firmly established driving forces of age-related CV dysfunction, also play an important role in atherosclerotic plaque destabilization and rupture. Several genes involved in lifespan determination are known regulator of redox cellular balance and pre-clinical evidence underlines their pathophysiological roles in age-related cardiovascular dysfunction and atherosclerosis. Objective: The aim of this narrative review is to examine the impact of aging on arterial function and atherosclerotic plaque development. Furthermore, we report how molecular mechanisms of vascular aging might regulate age-related plaque modifications and how this may help to identify novel therapeutic targets to attenuate the increased risk of CV disease in elderly people.

Molecular Mechanisms of Complement System Proteins and Matrix Metalloproteinases in the Pathogenesis of Age-Related Macular Degeneration

2019 ◽  
Vol 19 (10) ◽  
pp. 705-718 ◽  
Author(s):  
Naima Mansoor ◽  
Fazli Wahid ◽  
Maleeha Azam ◽  
Khadim Shah ◽  
Anneke I. den Hollander ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Macular Degeneration ◽  
Complement System ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Age Related Macular Degeneration ◽  
Genetic Changes ◽  
Complement System Proteins ◽  
Age Related ◽  
Common Genetic Variants

: Age-related macular degeneration (AMD) is an eye disorder affecting predominantly the older people above the age of 50 years in which the macular region of the retina deteriorates, resulting in the loss of central vision. The key factors associated with the pathogenesis of AMD are age, smoking, dietary, and genetic risk factors. There are few associated and plausible genes involved in AMD pathogenesis. Common genetic variants (with a minor allele frequency of >5% in the population) near the complement genes explain 40–60% of the heritability of AMD. The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. Genetic changes in and around several complement system genes, including the CFH, contribute to the formation of drusen and progression of AMD. Similarly, Matrix metalloproteinases (MMPs) that are normally involved in tissue remodeling also play a critical role in the pathogenesis of AMD. MMPs are involved in the degradation of cell debris and lipid deposits beneath retina but with age their functions get affected and result in the drusen formation, succeeding to macular degeneration. In this review, AMD pathology, existing knowledge about the normal and pathological role of complement system proteins and MMPs in the eye is reviewed. The scattered data of complement system proteins, MMPs, drusenogenesis, and lipofusogenesis have been gathered and discussed in detail. This might add new dimensions to the understanding of molecular mechanisms of AMD pathophysiology and might help in finding new therapeutic options for AMD.

Review of the Literature Examining the Association of Serum Uric Acid with Osteoporosis and Mechanistic Insights into Its Effect on Bone Metabolism

2019 ◽  
Vol 19 (3) ◽  
pp. 259-273 ◽  
Author(s):  
Neelam Kaushal ◽  
Divya Vohora ◽  
Rajinder K Jalali ◽  
Sujeet Jha
Keyword(s):  
Risk Factors ◽  
Bone Mineral Density ◽  
Uric Acid ◽  
Bone Metabolism ◽  
Serum Uric Acid ◽  
Bone Mineral ◽  
Molecular Mechanisms ◽  
Association Studies ◽  
Mineral Density ◽  
Age Related

Background And Objective:Osteoporosis is a common bone disorder that increases susceptibility to fragility bone fractures. The clinical and public health repercussions of osteoporosis are huge due to the morbidity, mortality, and cost of medical care linked with fragility fractures. Clinical assessment of osteoporotic risk factors can help to identify candidates at an early stage that will benefit from medical intervention and potentially lowering the morbidity and mortality seen with fractures and complications. Given this, research is ongoing to evaluate the association of osteoporosis with some novel or less well-studied risk factors/bio-markers such as uric acid (UA).Discussion:Uric acid’s antioxidant activity has been proposed to be one of the factors responsible for increasing longevity and lowering rates of age-related cancers during primate evolution, the level of which increased markedly due to loss of uricase enzyme activity (mutational silencing). Accumulated evidence shows that oxidative stress is the fundamental mechanism of age-related bone loss and acts via enhancing osteoclastic activity and increasing bone resorption. Antioxidant substances such as ascorbic acid scavenge free radicals are positively related to bone health. Thus, it is hypothesized that uric acid holds bone-protective potential owing to its potent antioxidative property. Several correlation studies have been conducted globally to investigate the relationship between serum uric acid with bone mineral density and osteoporosis. Few pre-clinical studies have tried to investigate the interaction between uric acid and bone mineral density and reported important role played via Runt-related transcription factor 2 (RUNX2)/core-binding factor subunit alpha-1 (CBF-alpha-1), Wingless-related integration site (Wnt)-3a/β-catenin signaling pathway and 11β Hydroxysteroid Dehydrogenase type 1.Conclusion:In this review, the authors provided a comprehensive summary of the literature related to association studies reported in humans as well work done until date to understand the potential cellular and molecular mechanisms that interplay between uric acid and bone metabolism.

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