scholarly journals A Network of Pathways Controlling Cellular Homeostasis Affects the Onset of Senescence in Podospora anserina

2021 ◽  
Vol 7 (4) ◽  
pp. 263
Author(s):  
Heinz D. Osiewacz ◽  
Lea Schürmanns
Keyword(s):  
Critical Issue ◽  
Podospora Anserina ◽  
Biological Aging ◽  
Oxygen Species ◽  
Cellular Homeostasis ◽  
The Past ◽  
Age Related ◽  
Molecular Damage ◽  
Different Levels ◽  
Critical Limits

Research on Podospora anserina unraveled a network of molecular pathways affecting biological aging. In particular, a number of pathways active in the control of mitochondria were identified on different levels. A long-known key process active during aging of P. anserina is the age-related reorganization of the mitochondrial DNA (mtDNA). Mechanisms involved in the stabilization of the mtDNA lead to lifespan extension. Another critical issue is to balance mitochondrial levels of reactive oxygen species (ROS). This is important because ROS are essential signaling molecules, but at increased levels cause molecular damage. At a higher level of the network, mechanisms are active in the repair of damaged compounds. However, if damage passes critical limits, the corresponding pathways are overwhelmed and impaired molecules as well as those present in excess are degraded by specific enzymes or via different forms of autophagy. Subsequently, degraded units need to be replaced by novel functional ones. The corresponding processes are dependent on the availability of intact genetic information. Although a number of different pathways involved in the control of cellular homeostasis were uncovered in the past, certainly many more exist. In addition, the signaling pathways involved in the control and coordination of the underlying pathways are only initially understood. In some cases, like the induction of autophagy, ROS are active. Additionally, sensing and signaling the energetic status of the organism plays a key role. The precise mechanisms involved are elusive and remain to be elucidated.

scholarly journals Mitochondria and Aging—The Role of Exercise as a Countermeasure

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 40 ◽  
Author(s):  
Mats I Nilsson ◽  
Mark A Tarnopolsky
Keyword(s):  
Reactive Oxygen Species Generation ◽  
Biological Aging ◽  
Primary Role ◽  
Oxygen Species ◽  
Vicious Cycle ◽  
Life And Death ◽  
Cell Functions ◽  
Age Related ◽  
Damage Protein

Mitochondria orchestrate the life and death of most eukaryotic cells by virtue of their ability to supply adenosine triphosphate from aerobic respiration for growth, development, and maintenance of the ‘physiologic reserve’. Although their double-membrane structure and primary role as ‘powerhouses of the cell’ have essentially remained the same for ~2 billion years, they have evolved to regulate other cell functions that contribute to the aging process, such as reactive oxygen species generation, inflammation, senescence, and apoptosis. Biological aging is characterized by buildup of intracellular debris (e.g., oxidative damage, protein aggregates, and lipofuscin), which fuels a ‘vicious cycle’ of cell/DNA danger response activation (CDR and DDR, respectively), chronic inflammation (‘inflammaging’), and progressive cell deterioration. Therapeutic options that coordinately mitigate age-related declines in mitochondria and organelles involved in quality control, repair, and recycling are therefore highly desirable. Rejuvenation by exercise is a non-pharmacological approach that targets all the major hallmarks of aging and extends both health- and lifespan in modern humans.

scholarly journals Production, Signaling, and Scavenging Mechanisms of Reactive Oxygen Species in Fruit–Pathogen Interactions

2019 ◽  
Vol 20 (12) ◽  
pp. 2994 ◽  
Author(s):  
Ying Wang ◽  
Dongchao Ji ◽  
Tong Chen ◽  
Boqiang Li ◽  
Zhanquan Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Pathogenic Fungi ◽  
Ros Production ◽  
Oxygen Species ◽  
Ros Homeostasis ◽  
Molecular Damage ◽  
Different Levels ◽  
In Cells

Reactive oxygen species (ROS) play a dual role in fruit–pathogen interaction, which largely depends on their different levels in cells. Fruit recognition of a pathogen immediately triggers an oxidative burst that is considered an integral part of the fruit defense response. ROS are also necessary for the virulence of pathogenic fungi. However, the accumulation of ROS in cells causes molecular damage and finally leads to cell death. In this review, on the basis of data regarding ROS production and the scavenging systems determining ROS homeostasis, we focus on the role of ROS in fruit defense reactions against pathogens and in fungi pathogenicity during fruit–pathogen interaction.

scholarly journals Regular and Moderate Exercise Counteracts the Decline of Antioxidant Protection but Not Methylglyoxal-Dependent Glycative Burden in the Ovary of Reproductively Aging Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
S. Falone ◽  
S. Jr Santini ◽  
V. Cordone ◽  
M. Grannonico ◽  
M. Cacchio ◽  
...  
Keyword(s):  
Healthy Aging ◽  
Molecular Mechanisms ◽  
Population Aging ◽  
Oxygen Species ◽  
Moderate Exercise ◽  
Mouse Ovary ◽  
Age Related ◽  
Age Dependent ◽  
Molecular Damage

Population aging results in urgent needs of interventions aimed at ensuring healthy senescence. Exercise often results in healthy aging, yet many molecular mechanisms underlying such effects still need to be identified. We here investigated whether the age-dependent accumulation of oxidative and methylglyoxal- (MG-) related molecular damage could be delayed by moderate exercise in the mouse ovary, an organ that first exhibits impaired function with advancing age in mammals. CD1 female mice underwent two- or four-month treadmill-based running through the transition from adult to middle age, when ovaries show signs of senescence, and markers of protection against reactive oxygen species (ROS) and MG were measured. The long-term exercise reduced the protein oxidative damage in the ovaries (P<0.01), and this was linked to the preservation of the glutathione peroxidase protection against ROS (P<0.001), as well as to the increased glutathione availability (P<0.001). Conversely, even though the age-related deactivation of the MG-targeting systems was partially prevented by the long-term running programme (P<0.001), exercised mice were not protected from the age-dependent glycative burden. In summary, lately initiated regular and moderate exercise limited some changes occurring in the ovaries of middle-aged mice, and this might help to develop nonpharmacological cointerventions to reduce the vulnerability of mammalian ovaries towards redox dysfunctions.

scholarly journals Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Redox Status ◽  
The Body ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Enzymatic Production ◽  
Age Related ◽  
Anti Oxidant ◽  
Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

scholarly journals Nanoceria Prevents Glucose-Induced Protein Glycation in Eye Lens Cells

Nanomaterials ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1473
Author(s):  
Belal I. Hanafy ◽  
Gareth W. V. Cave ◽  
Yvonne Barnett ◽  
Barbara K. Pierscionek
Keyword(s):  
Protein Glycation ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Oxide Nanoparticles ◽  
Lens Protein ◽  
Oxygen Species ◽  
Human Lens Epithelial Cells ◽  
Age Related ◽  
Age Related Changes

Cerium oxide nanoparticles (nanoceria) are generally known for their recyclable antioxidative properties making them an appealing biomaterial for protecting against physiological and pathological age-related changes that are caused by reactive oxygen species (ROS). Cataract is one such pathology that has been associated with oxidation and glycation of the lens proteins (crystallins) leading to aggregation and opacification. A novel coated nanoceria formulation has been previously shown to enter the human lens epithelial cells (HLECs) and protect them from oxidative stress induced by hydrogen peroxide (H2O2). In this work, the mechanism of nanoceria uptake in HLECs is studied and multiple anti-cataractogenic properties are assessed in vitro. Our results show that the nanoceria provide multiple beneficial actions to delay cataract progression by (1) acting as a catalase mimetic in cells with inhibited catalase, (2) improving reduced to oxidised glutathione ratio (GSH/GSSG) in HLECs, and (3) inhibiting the non-enzymatic glucose-induced glycation of the chaperone lens protein α-crystallin. Given the multifactorial nature of cataract progression, the varied actions of nanoceria render them promising candidates for potential non-surgical therapeutic treatment.

scholarly journals Stiffness and Aging in Cardiovascular Diseases: The Dangerous Relationship between Force and Senescence

2021 ◽  
Vol 22 (7) ◽  
pp. 3404
Author(s):  
Silvia Ferrari ◽  
Maurizio Pesce
Keyword(s):  
Risk Factors ◽  
Aging Process ◽  
Tissue Structure ◽  
Biological Aging ◽  
Ros Production ◽  
Oxygen Species ◽  
Chromatin Modifications ◽  
Gradual Decline ◽  
Cycle Arrest ◽  
Inflammatory Activation

Biological aging is a process associated with a gradual decline in tissues’ homeostasis based on the progressive inability of the cells to self-renew. Cellular senescence is one of the hallmarks of the aging process, characterized by an irreversible cell cycle arrest due to reactive oxygen species (ROS) production, telomeres shortening, chronic inflammatory activation, and chromatin modifications. In this review, we will describe the effects of senescence on tissue structure, extracellular matrix (ECM) organization, and nucleus architecture, and see how these changes affect (are affected by) mechano-transduction. In our view, this is essential for a deeper understanding of the progressive pathological evolution of the cardiovascular system and its relationship with the detrimental effects of risk factors, known to act at an epigenetic level.

scholarly journals Age-Related Macular Degeneration: Role of Oxidative Stress and Blood Vessels

2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Therapeutic Strategies ◽  
Vision Impairment ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Age Related

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.

Effects of age and maternal reactivity on the stress response of the pituitary-adrenocortical axis and the sympathetic nervous system in neonatal pigs

1999 ◽  
Vol 68 (3) ◽  
pp. 519-526 ◽  
Author(s):  
E. Kanitz ◽  
W. Otten ◽  
G. Nürnberg ◽  
K. P. Brüssow
Keyword(s):  
Stress Reactivity ◽  
Acth Stimulation Test ◽  
Acth Stimulation ◽  
Acth Challenge ◽  
Neonatal Pigs ◽  
Age Related ◽  
Highly Sensitive ◽  
Function Test ◽  
Adrenal Response ◽  
Different Levels

AbstractThe study was conducted to investigate the adreno cortical capacity after injection of ACTH and the sensitivity of the pituitary and the adrenal to immobilization in neonatal pigs at different ages. Furthermore, the endocrine reactivity of the offspring was compared with the stress reactivity of their mothers. Four piglets were selected from each of six different litters and subjected to an immobilization test and an adrenal function test using synthetic ACTH1-24 at the ages of 7, 21 and 35 days; the six sows were also subjected to restraint and an ACTH stimulation test. Plasma β-endorphin, norepinephrine and epinephrine concentrations were measured in blood samples taken 2 min after restraint and cortisol concentrations were measured 60 min after ACTH administration. A highly sensitive adrenal response was demonstrated in both sows and piglets and adrenal reactivity showed also a considerable consistency over time within sows. In neonatal pigs, the cortisol response to ACTH was greatest on day 7 and decreased up to day 35. Plasma epinephrine and norepinephrine levels after the 2-min immobilization were also higher at day 7 compared with the other ages (P < 0·01). Piglets from sows, classified as high reacting according to their cortisol or epinephrine response, also showed significantly higher cortisol levels after ACTH challenge at all ages and significantly higher epinephrine levels after restraint at day 7 than piglets from low reacting sows. The results show an age-related change of pituitary-adrenocortical and sympatho-adrenomedullary responses in neonatal pigs and an absence of a stress hyporesponsive period at all ages studied. The results also indicate different levels of excitability in the offspring depending on the maternal stress reactivity.

scholarly journals Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice

2021 ◽  
Vol 22 (7) ◽  
pp. 3548
Author(s):  
Kenji Watanabe ◽  
Shuichi Shibuya ◽  
Yusuke Ozawa ◽  
Toshihiko Toda ◽  
Takahiko Shimizu
Keyword(s):  
Apoptotic Cell ◽  
Oxygen Species ◽  
Double Knockout ◽  
In Vivo Experiments ◽  
P53 Signaling ◽  
Tissue Degeneration ◽  
Age Related ◽  
Tissue Changes ◽  
P53 Activation

Intracellular superoxide dismutases (SODs) maintain tissue homeostasis via superoxide metabolism. We previously reported that intracellular reactive oxygen species (ROS), including superoxide accumulation caused by cytoplasmic SOD (SOD1) or mitochondrial SOD (SOD2) insufficiency, induced p53 activation in cells. SOD1 loss also induced several age-related pathological changes associated with increased oxidative molecules in mice. To evaluate the contribution of p53 activation for SOD1 knockout (KO) (Sod1−/−) mice, we generated SOD1 and p53 KO (double-knockout (DKO)) mice. DKO fibroblasts showed increased cell viability with decreased apoptosis compared with Sod1−/− fibroblasts. In vivo experiments revealed that p53 insufficiency was not a great contributor to aging-like tissue changes but accelerated tumorigenesis in Sod1−/− mice. Furthermore, p53 loss failed to improve dilated cardiomyopathy or the survival in heart-specific SOD2 conditional KO mice. These data indicated that p53 regulated ROS-mediated apoptotic cell death and tumorigenesis but not ROS-mediated tissue degeneration in SOD-deficient models.

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