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.

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.

scholarly journals Lysosomal Exocytosis, Exosome Release and Secretory Autophagy: The Autophagic- and Endo-Lysosomal Systems Go Extracellular

2020 ◽  
Vol 21 (7) ◽  
pp. 2576 ◽  
Author(s):  
Sandra Buratta ◽  
Brunella Tancini ◽  
Krizia Sagini ◽  
Federica Delo ◽  
Elisabetta Chiaradia ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Cell Communication ◽  
Lysosomal Storage ◽  
Cellular Processes ◽  
Age Related ◽  
Extracellular Release ◽  
A Cell ◽  
Endosomal System

Beyond the consolidated role in degrading and recycling cellular waste, the autophagic- and endo-lysosomal systems play a crucial role in extracellular release pathways. Lysosomal exocytosis is a process leading to the secretion of lysosomal content upon lysosome fusion with plasma membrane and is an important mechanism of cellular clearance, necessary to maintain cell fitness. Exosomes are a class of extracellular vesicles originating from the inward budding of the membrane of late endosomes, which may not fuse with lysosomes but be released extracellularly upon exocytosis. In addition to garbage disposal tools, they are now considered a cell-to-cell communication mechanism. Autophagy is a cellular process leading to sequestration of cytosolic cargoes for their degradation within lysosomes. However, the autophagic machinery is also involved in unconventional protein secretion and autophagy-dependent secretion, which are fundamental mechanisms for toxic protein disposal, immune signalling and pathogen surveillance. These cellular processes underline the crosstalk between the autophagic and the endosomal system and indicate an intersection between degradative and secretory functions. Further, they suggest that the molecular mechanisms underlying fusion, either with lysosomes or plasma membrane, are key determinants to maintain cell homeostasis upon stressing stimuli. When they fail, the accumulation of undigested substrates leads to pathological consequences, as indicated by the involvement of autophagic and lysosomal alteration in human diseases, namely lysosomal storage disorders, age-related neurodegenerative diseases and cancer. In this paper, we reviewed the current knowledge on the functional role of extracellular release pathways involving lysosomes and the autophagic- and endo-lysosomal systems, evaluating their implication in health and disease.

scholarly journals Do Nutritional Supplements Have a Role in Age Macular Degeneration Prevention?

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Maria D. Pinazo-Durán ◽  
Francisco Gómez-Ulla ◽  
Luis Arias ◽  
Javier Araiz ◽  
Ricardo Casaroli-Marano ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Scientific Evidence ◽  
Experimental Studies ◽  
Beta Carotene ◽  
Dietary Intakes ◽  
Omega 3 ◽  
Age Related ◽  
Disease Study

Purpose. To review the proposed pathogenic mechanisms of age macular degeneration (AMD), as well as the role of antioxidants (AOX) and omega-3 fatty acids (ω-3) supplements in AMD prevention.Materials and Methods. Current knowledge on the cellular/molecular mechanisms of AMD and the epidemiologic/experimental studies on the effects of AOX andω-3 were addressed all together with the scientific evidence and the personal opinion of professionals involved in the Retina Group of the OFTARED (Spain).Results. High dietary intakes ofω-3 and macular pigments lutein/zeaxanthin are associated with lower risk of prevalence and incidence in AMD. The Age-Related Eye Disease study (AREDS) showed a beneficial effect of high doses of vitamins C, E, beta-carotene, and zinc/copper in reducing the rate of progression to advanced AMD in patients with intermediate AMD or with one-sided late AMD. The AREDS-2 study has shown that lutein and zeaxanthin may substitute beta-carotene because of its potential relationship with increased lung cancer incidence.Conclusion. Research has proved that elder people with poor diets, especially with low AOX andω-3 micronutrients intake and subsequently having low plasmatic levels, are more prone to developing AMD. Micronutrient supplementation enhances antioxidant defense and healthy eyes and might prevent/retard/modify AMD.

scholarly journals Thrombospondin-1 in maladaptive aging responses: a concept whose time has come

2020 ◽  
Vol 319 (1) ◽  
pp. C45-C63
Author(s):  
Jeffrey S. Isenberg ◽  
David D. Roberts
Keyword(s):  
Molecular Mechanisms ◽  
Synapse Formation ◽  
Genotoxic Stress ◽  
Cell Types ◽  
Cellular Tissue ◽  
Therapeutic Agents ◽  
Age Related ◽  
Organ Systems ◽  
Age Dependent ◽  
Thrombospondin 1

Numerous age-dependent alterations at the molecular, cellular, tissue and organ systems levels underlie the pathophysiology of aging. Herein, the focus is upon the secreted protein thrombospondin-1 (TSP1) as a promoter of aging and age-related diseases. TSP1 has several physiological functions in youth, including promoting neural synapse formation, mediating responses to ischemic and genotoxic stress, minimizing hemorrhage, limiting angiogenesis, and supporting wound healing. These acute functions of TSP1 generally require only transient expression of the protein. However, accumulating basic and clinical data reinforce the view that chronic diseases of aging are associated with accumulation of TSP1 in the extracellular matrix, which is a significant maladaptive contributor to the aging process. Identification of the relevant cell types that chronically produce and respond to TSP1 and the molecular mechanisms that mediate the resulting maladaptive responses could direct the development of therapeutic agents to delay or revert age-associated maladies.

scholarly journals Regulation of Autophagy in Aging and Disease

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 743-744
Author(s):  
Malene Hansen
Keyword(s):  
Molecular Mechanisms ◽  
Molecular Level ◽  
Recycling Process ◽  
Cellular Homeostasis ◽  
C Elegans ◽  
Age Related ◽  
Multiple Levels ◽  
Critical Process

Abstract The cytosolic recycling process of autophagy plays an important role in many age-related diseases and has been directly linked to aging, including in the nematode C. elegans where autophagy appears beneficially induced in many conserved longevity models. As a critical process to ensure cellular homeostasis, autophagy is regulated at multiple levels, yet it remains a challenge in the field to understand how the regulation of autophagy is integrated at the cellular and molecular level to ensure health- and lifespan benefits. I will here discuss our progress on understanding the different molecular mechanisms employed by cells and organisms to regulate autophagy in response to stressors such as aging and disease.

Nutritional Aspects of Spermidine

2020 ◽  
Vol 40 (1) ◽  
pp. 135-159 ◽  
Author(s):  
Frank Madeo ◽  
Sebastian J. Hofer ◽  
Tobias Pendl ◽  
Maria A. Bauer ◽  
Tobias Eisenberg ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Epidemiological Studies ◽  
Preclinical Models ◽  
Cellular Functions ◽  
Age Related ◽  
Specific Manner ◽  
Age Dependent ◽  
Cell Type Specific ◽  
Positively Charged ◽  
Overall Mortality

Natural polyamines (spermidine and spermine) are small, positively charged molecules that are ubiquitously found within organisms and cells. They exert numerous (intra)cellular functions and have been implicated to protect against several age-related diseases. Although polyamine levels decline in a complex age-dependent, tissue-, and cell type–specific manner, they are maintained in healthy nonagenarians and centenarians. Increased polyamine levels, including through enhanced dietary intake, have been consistently linked to improved health and reduced overall mortality. In preclinical models, dietary supplementation with spermidine prolongs life span and health span. In this review, we highlight salient aspects of nutritional polyamine intake and summarize the current knowledge of organismal and cellular uptake and distribution of dietary (and gastrointestinal) polyamines and their impact on human health. We further summarize clinical and epidemiological studies of dietary polyamines.

scholarly journals Hypertrophic Scarring: Current Knowledge of Predisposing Factors, Cellular and Molecular Mechanisms

2020 ◽  
Vol 41 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Layla Nabai ◽  
Amir Pourghadiri ◽  
Aziz Ghahary
Keyword(s):  
Molecular Mechanisms ◽  
Molecular Level ◽  
Current Knowledge ◽  
Wound Care ◽  
Surgical Techniques ◽  
Predisposing Factors ◽  
Hypertrophic Scarring ◽  
Prevention And Treatment ◽  
Therapeutic Measures

Abstract Hypertrophic scarring (HSc) is an age-old problem that still affects millions of people physically, psychologically, and economically. Despite advances in surgical techniques and wound care, prevention and treatment of HSc remains a challenge. Elucidation of factors involved in the development of this common fibroproliferative disorder is crucial for further progress in preventive and/or therapeutic measures. Our knowledge about pathophysiology of HSc at the cellular and molecular level has grown considerably in recent decades. In this article, current knowledge of predisposing factors and the cellular and molecular mechanisms of HSc has been reviewed.

scholarly journals The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis

2010 ◽  
Vol 205 (3) ◽  
pp. 201-210 ◽  
Author(s):  
Sebastio Perrini ◽  
Luigi Laviola ◽  
Marcos C Carreira ◽  
Angelo Cignarelli ◽  
Annalisa Natalicchio ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Signs And Symptoms ◽  
Well Being ◽  
Serum Levels ◽  
Normal Range ◽  
Gh Secretion ◽  
Skeletal Muscle Wasting ◽  
Age Related ◽  
Age Dependent

The widespread increase in life expectancy is accompanied by an increased prevalence of features of physical frailty. Signs and symptoms may include sarcopenia and osteopenia, reduced exercise capacity, and diminished sense of well-being. The pathogenesis of age-associated sarcopenia and osteopenia is multifactorial, and hormonal decline may be a contributing factor. Aging is associated with a progressive decrease in GH secretion, and more than 30% of elderly people have circulating IGF1 levels below the normal range found in the young. GH acts directly on target tissues, including skeletal muscle and bone among many others, but many effects are mediated indirectly by circulating (liver-derived) or locally produced IGF1. Aging is also associated with reduced insulin sensitivity which, in turn, may contribute to the impairment of IGF1 action. Recent experimental evidence suggests that besides the age-dependent decline in GH and IGF1 serum levels, the dysregulation of GH and IGF1 actions due to impairment of the post-receptor signaling machinery may contribute to the loss of muscle mass and osteopenia. This article will focus on the molecular mechanisms of impaired GH and IGF1 signaling and action in aging, and their role in the pathogenesis of sarcopenia and osteoporosis.

scholarly journals MECHANISMS OF BRAIN REJUVENATION

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S587-S587
Author(s):  
Saul Villeda
Keyword(s):  
Molecular Mechanisms ◽  
Aging Brain ◽  
Aging Effects ◽  
Effective Strategies ◽  
Mechanistic Insight ◽  
Age Related ◽  
Age Dependent ◽  
Cognitive Faculties ◽  
Insight Into ◽  
Aging Factors

Abstract A growing body of work has shown that systemic manipulations, such as heterochronic parabiosis and young blood administration, can partially reverse age-related cellular impairments and loss of cognitive faculties in the aged brain. These studies have revealed an age-dependent bi-directionality in the influence of the systemic environment indicating anti-aging factors in young blood elicit rejuvenation while pro-aging factors in old blood drive aging. It has been proposed that introducing anti-aging factors or mitigating the effect of pro-aging factors may provide effective strategies to rejuvenate aging phenotypes. Despite this potential, much is unknown as to the systemic and molecular mechanisms regulating anti-aging and pro-aging effects of blood-borne factors. I will discuss work from my research group that begins to provide mechanistic insight into the systemic and molecular drivers promoting rejuvenation in the aging brain.

scholarly journals Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

2021 ◽  
Vol 22 (8) ◽  
pp. 4052
Author(s):  
Kévin Nay ◽  
William J. Smiles ◽  
Jacqueline Kaiser ◽  
Luke M. McAloon ◽  
Kim Loh ◽  
...  
Keyword(s):  
Brain Function ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Well Being ◽  
Developed Countries ◽  
Beneficial Effects ◽  
Therapeutic Benefits ◽  
Age Related ◽  
Underlying Mechanisms ◽  
The Impact

As life expectancy has increased, particularly in developed countries, due to medical advances and increased prosperity, age-related neurological diseases and mental health disorders have become more prevalent health issues, reducing the well-being and quality of life of sufferers and their families. In recent decades, due to reduced work-related levels of physical activity, and key research insights, prescribing adequate exercise has become an innovative strategy to prevent or delay the onset of these pathologies and has been demonstrated to have therapeutic benefits when used as a sole or combination treatment. Recent evidence suggests that the beneficial effects of exercise on the brain are related to several underlying mechanisms related to muscle–brain, liver–brain and gut–brain crosstalk. Therefore, this review aims to summarize the most relevant current knowledge of the impact of exercise on mood disorders and neurodegenerative diseases, and to highlight the established and potential underlying mechanisms involved in exercise–brain communication and their benefits for physiology and brain function.

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