scholarly journals Mitochondrial transformations in the aging human placenta

2020 ◽  
Vol 319 (6) ◽  
pp. E981-E994
Author(s):  
Lucy A. Bartho ◽  
Joshua J. Fisher ◽  
James S. M. Cuffe ◽  
Anthony V. Perkins
Keyword(s):  
Human Placenta ◽  
Cell Biology ◽  
Later Life ◽  
Cellular Damage ◽  
Gestational Length ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Cellular Environment ◽  
Age Related ◽  
And Function

Mitochondria play a key role in homeostasis and are central to one of the leading hypotheses of aging, the free radical theory. Mitochondria function as a reticulated network, constantly adapting to the cellular environment through fusion (joining), biogenesis (formation of new mitochondria), and fission (separation). This adaptive response is particularly important in response to oxidative stress, cellular damage, and aging, when mitochondria are selectively removed through mitophagy, a mitochondrial equivalent of autophagy. During this complex process, mitochondria influence surrounding cell biology and organelles through the release of signaling molecules. Given that the human placenta is a unique organ having a transient and somewhat defined life span of ∼280 days, any adaption or dysfunction associated with mitochondrial physiology as a result of aging will have a dramatic impact on the health and function of both the placenta and the fetus. Additionally, a defective placenta during gestation, resulting in reduced fetal growth, has been shown to influence the development of chronic disease in later life. In this review we focus on the mitochondrial adaptions and transformations that accompany gestational length and share similarities with age-related diseases. In addition, we discuss the role of such changes in regulating placental function throughout gestation, the etiology of gestational complications, and the development of chronic diseases later in life.

scholarly journals Membrane-associated phase separation: organization and function emerge from a two-dimensional milieu

2021 ◽  
Author(s):  
Jonathon A Ditlev
Keyword(s):  
Phase Separation ◽  
Cell Biology ◽  
Cellular Environment ◽  
Condensate Formation ◽  
Associated Proteins ◽  
Available Technology ◽  
And Function ◽  
Surrounding Membrane

Abstract Liquid‒liquid phase separation (LLPS) of biomolecules has emerged as an important mechanism that contributes to cellular organization. Phase separated biomolecular condensates, or membrane-less organelles, are compartments composed of specific biomolecules without a surrounding membrane in the nucleus and cytoplasm. LLPS also occurs at membranes, where both lipids and membrane-associated proteins can de-mix to form phase separated compartments. Investigation of these membrane-associated condensates using in vitro biochemical reconstitution and cell biology has provided key insights into the role of phase separation in membrane domain formation and function. However, these studies have generally been limited by available technology to study LLPS on model membranes and the complex cellular environment that regulates condensate formation, composition, and function. Here, I briefly review our current understanding of membrane-associated condensates, establish why LLPS can be advantageous for certain membrane-associated condensates, and offer a perspective for how these condensates may be studied in the future.

scholarly journals Effects of Caloric Restriction on Cardiac Oxidative Stress and Mitochondrial Bioenergetics: Potential Role of Cardiac Sirtuins

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ken Shinmura
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Caloric Restriction ◽  
Functional Decline ◽  
Cellular Damage ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Stress Theory

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.

scholarly journals LIFE COURSE ORIGINS OF FRAILTY IN LATER LIFE

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S59-S59
Author(s):  
Monica Williams-Farrelly ◽  
Kenneth F Ferraro
Keyword(s):  
Health Outcomes ◽  
Parental Behavior ◽  
Later Life ◽  
Clinical State ◽  
Adult Health ◽  
Logistic Regression Models ◽  
Health Outcomes Research ◽  
Age Related ◽  
And Function ◽  
Retirement Study

Abstract Frailty, generally characterized as a clinical state of increased vulnerability resulting from age-related decline in reserve and function across multiple physiologic systems, has been gaining attention in recent years due to its high correlates with a number of poor health outcomes including falls, hospitalization, and mortality. Similar to other adult health outcomes, research on the etiology of frailty has begun to move from proximal risk factors only to those more distal in time. This research uses data from the Health and Retirement study (2004-2016) to examine whether childhood exposures predict developing frailty in later life. A series of ordinal logistic regression models were estimated to test whether six domains of childhood exposures (socioeconomic status, infectious disease, chronic disease, impairments, risky adolescent behavior, and risky parental behavior) were associated with frailty, composed of five components: unintentional weight loss, weakness, slowness, exhaustion, and low energy expenditure (Fried et al., 2001). After adjusting for demographic factors, experiencing multiple SES misfortunes or risky adolescent behaviors in childhood are associated with higher odds of frailty in later life (OR= 1.24 and 2.37, respectively), while experiencing any infectious diseases is associated with lower odds of frailty (OR= 0.67 and 0.72). After further adjusting for adult characteristics, experiencing 2 or more chronic diseases in childhood is associated with a 1.35 higher odds of incident frailty over an 8-year period. These results reveal some of the early exposures that may raise frailty risk in later life but also the mid-life factors that mediate those risks.

Biology of Aging

2018 ◽  
Author(s):  
Deepak Bharadia ◽  
Raquel Minasian ◽  
Indranil Sinha
Keyword(s):  
Soft Tissue ◽  
The Elderly ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Care For The Elderly ◽  
Age Related ◽  
Clinical Scenarios ◽  
Specific Tissue ◽  
Biology Of Aging ◽  
Age Related Changes

With aging, there are multiple internal and external factors that are associated with age-related changes in skin and soft tissue.  As Plastic Surgeons, we very commonly evaluate and treat elderly patients, often offering ‘anti-aging’ treatments.  An understanding of the science behind aging as well as common patterns of change seen in soft tissue may allow us to refine our treatments.  This review provides an overview of mechanisms underlying aging, as well common clinical scenarios with aging regarding anatomic sites commonly treated by Plastic Surgeons including the face, breast, and abdomen.  Separately, we discuss aging associated changes to specific tissue types, including skin, fat, muscle, and bone.  Knowledge of factors related to aging and concepts related to safe interventions to reverse or mitigate age-related changes and integral to our ability to care for the elderly population.   This review contains 9 figures, 3 tables and 69 references Key Words : Cellular senescence, mitochondrial theory, free radical theory, inflammation, protein damage hypothesis, glycation hypothesis, atrophy, lipotoxicity, rhytids, involution  

scholarly journals Markers of Oxidative Stress in Erythrocytes and Plasma During Aging in Humans

2010 ◽  
Vol 3 (1) ◽  
pp. 2-12 ◽  
Author(s):  
Kanti Bhooshan Pandey ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Biological Process ◽  
Related Phenomenon ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Age Related ◽  
General Decline ◽  
Markers Of Oxidative Stress ◽  
Probability Of Death

Aging is an inevitable universal biological process, which can be characterized by a general decline in physiological function with the accumulation of diverse adverse changes and increased probability of death. Among several theories, oxidative stress/free radical theory offers the best mechanistic elucidation of the aging process and other age-related phenomenon. In the present paper, we discuss the aging process and have focused on the importance of some reliable markers of oxidative stress which may be used as biomarkers of the aging process.

scholarly journals MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Huaije Bu ◽  
Sophia Wedel ◽  
Maria Cavinato ◽  
Pidder Jansen-Dürr
Keyword(s):  
Oxidative Stress ◽  
Cellular Senescence ◽  
Cellular Tissue ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Microrna Regulation ◽  
Age Related ◽  
Epigenetic Events ◽  
Permanent Cell ◽  
Theory Of Aging

Aging is a time-related process of functional deterioration at cellular, tissue, organelle, and organismal level that ultimately brings life to end. Cellular senescence, a state of permanent cell growth arrest in response to cellular stress, is believed to be the driver of the aging process and age-related disorders. The free radical theory of aging, referred to as oxidative stress (OS) theory below, is one of the most studied aging promoting mechanisms. In addition, genetics and epigenetics also play large roles in accelerating and/or delaying the onset of aging and aging-related diseases. Among various epigenetic events, microRNAs (miRNAs) turned out to be important players in controlling OS, aging, and cellular senescence. miRNAs can generate rapid and reversible responses and, therefore, are ideal players for mediating an adaptive response against stress through their capacity to fine-tune gene expression. However, the importance of miRNAs in regulating OS in the context of aging and cellular senescence is largely unknown. The purpose of our article is to highlight recent advancements in the regulatory role of miRNAs in OS-induced cellular senescence.

scholarly journals ADAM17-triggered TNF signalling protects the ageing Drosophila retina from lipid droplet mediated degeneration

2020 ◽  
Author(s):  
Sonia Muliyil ◽  
Clémence Levet ◽  
Stefan Düsterhöft ◽  
Iqbal Dulloo ◽  
Sally Cowley ◽  
...  
Keyword(s):  
Lipid Droplet ◽  
Tumour Necrosis ◽  
Later Life ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Tnf Receptor ◽  
Age Related ◽  
Abnormal Accumulation ◽  
Necrosis Factor ◽  
Tnf Tumour Necrosis Factor

AbstractAnimals have evolved multiple mechanisms to protect themselves from the cumulative effects of age-related cellular damage. Here we reveal an unexpected link between the TNF (tumour necrosis factor) inflammatory pathway, triggered by the metalloprotease ADAM17/TACE, and a lipid droplet (LD)-mediated mechanism of protecting retinal cells from age related degeneration. Loss of ADAM17, TNF and the TNF receptor Grindelwald in pigmented glial cells of the Drosophila retina leads to age related degeneration of both glia and neurons, preceded by an abnormal accumulation of glial LDs. We show that the glial LDs initially buffer the cells against damage caused by neuronally generated reactive oxygen species (ROS), but that in later life the LDs dissipate, leading to the release of toxic peroxidated lipids. Finally, we demonstrate the existence of a conserved pathway in human iPS-derived microglia-like cells, which are central players in neurodegeneration. Overall, we have discovered a pathway mediated by TNF signalling acting not as a trigger of inflammation, but as a cytoprotective factor in the retina.

scholarly journals Recent Review on Oxidative stress, Cellular senescence and Age-Associated Diseases

2020 ◽  
Vol 11 (2) ◽  
pp. 1331-1342
Author(s):  
Nandita H ◽  
Manohar M ◽  
Gowda DV
Keyword(s):  
Oxidative Stress ◽  
Cellular Senescence ◽  
Tumor Development ◽  
Cellular Level ◽  
The Novel ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Age Related ◽  
Theory Of Aging ◽  
Main Factor

Reactive Oxygen Species (ROS) is considered as the main factor of the Free Radical theory of aging over centuries and it indicates the pathophysiology of aging in mammals. ROS causes oxidative stress, which is a major component in the aging process of higher organisms. ROS also leads to many age-related diseases such as cancer, cardiovascular disease, diabetes, etc. ROS causes damage to most of the biological membranes that cause these chronic diseases. Enhanced ROS levels at the cellular level lead to cellular senescence. It is a stage of cells where growth arrest happens associated with the secretion of Senescence-associated secretory phenotype (SASP) factors. Senescence maintains tissue homeostasis, functions in normal development and restricts tumor development. In this regard, recent experimental evidence has shown that the genetic or pharmacological ablation of senescent cells extends the life span and improves the healthspan. Here, we review the cellular and molecular links between cellular senescence and aging and discuss the novel therapeutic avenues that this connection opens.

scholarly journals OXIDATIVE STRESS IN AGING

2020 ◽  
pp. 10-22
Author(s):  
Н. К. Зенков ◽  
П. М. Кожин ◽  
А. В. Чечушков ◽  
Н. В. Кандалинцева ◽  
Г. Г. Мартинович ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Redox Balance ◽  
Ros Generation ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Age Related ◽  
Theory Of Aging ◽  
Autophagy Activity ◽  
Important System

Выдвинутая более 50 лет назад Д. Харманом свободнорадикальная теория старения остается популярной и сегодня. В обзоре проведен анализ возрастных изменений основных эндогенных механизмов продукции активированных кислородных метаболитов (АКМ) и механизмов антиоксидантной защиты. С возрастом генерация АКМ митохондриями, пероксисомами и NAD(P) H -оксидазами усиливается, в то время как транскрипционная активность важной системы поддержания редокс-баланса Keap 1/ Nrf 2/ ARE уменьшается. У старых животных отмечается также низкая активность аутофагии, удаляющей из клеток поврежденные органеллы и агрегированные структуры. Возрастное смещение редокс-баланса в сторону окислительного стресса может являться причиной развития возраст-ассоциированных нейрогеденеративных, аутоиммунных и воспалительных патологий. The free-radical theory of aging, advanced more than 50 years ago by D. Harman, remains popular today. The review analyzes age-related changes in the main endogenous mechanisms of reactive oxygen species (ROS) production and antioxidant defense mechanisms. With age, ROS generation by mitochondria, peroxisomes, and NAD(P)H oxidases is enhanced, while the transcriptional activity of the important system Keap 1/ Nrf 2/ ARE maintaining redox balance decreases. In old animals, autophagy activity is also low, which removes damaged organelles and aggregated structures from cells. The age-related shift of the redox balance towards oxidative stress can cause the development of age-associated neurodegenerative, autoimmune and infl ammatory pathologies.

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