scholarly journals Mitochondrial Function and Mitophagy in the Elderly: Effects of Exercise

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Osvaldo C. Moreira ◽  
Brisamar Estébanez ◽  
Susana Martínez-Florez ◽  
José A. de Paz ◽  
María J. Cuevas ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Structural Integrity ◽  
Apoptotic Cell ◽  
The Elderly ◽  
Model Organisms ◽  
Beneficial Effects ◽  
Cell Life ◽  
Mitochondrial Functions ◽  
Quantity Control ◽  
Changes Over Time

Aging is a natural, multifactorial and multiorganic phenomenon wherein there are gradual physiological and pathological changes over time. Aging has been associated with a decrease of autophagy capacity and mitochondrial functions, such as biogenesis, dynamics, and mitophagy. These processes are essential for the maintenance of mitochondrial structural integrity and, therefore, for cell life, since mitochondrial dysfunction leads to an impairment of energy metabolism and increased production of reactive oxygen species, which consequently trigger mechanisms of cellular senescence and apoptotic cell death. Moreover, reduced mitochondrial function can contribute to age-associated disease phenotypes in model organisms and humans. Literature data show beneficial effects of exercise on the impairment of mitochondrial biogenesis and dynamics and on the decrease in the mitophagic capacity associated to aging. Thus, exercise could have effects on the major cell signaling pathways that are involved in the mitochondria quality and quantity control in the elderly. Although it is known that several exercise protocols are able to modify the activity and turnover of mitochondria, further studies are necessary in order to better identify the mechanisms of interaction between mitochondrial functions, aging, and physical activity, as well as to analyze possible factors influencing these processes.

scholarly journals Mitochondrial Adaptations in Aged Skeletal Muscle: Effect of Exercise Training

2017 ◽  
pp. 1-14 ◽  
Author(s):  
M. M. ZIAALDINI ◽  
S. R. A. HOSSEINI ◽  
M. FATHI
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Function ◽  
The Elderly ◽  
Elderly Subjects ◽  
Cellular Mechanisms ◽  
Healthy Elderly ◽  
Mitochondrial Functions ◽  
Healthy Elderly Subjects ◽  
Mitochondrial Adaptations

The aging process is associated with a decline in mitochondrial functions. Mitochondria dysfunction is involved in initiation and progression of many health problems including neuromuscular, metabolic and cardiovascular diseases. It is well known that endurance exercise improves mitochondrial function, especially in the elderly. However, recent studies have demonstrated that resistance training lead also to substantial increases in mitochondrial function in skeletal muscle. A comprehensive understanding of the cellular mechanisms involved in the skeletal muscle mitochondrial adaptations to exercise training in healthy elderly subjects, can help practitioners to design and prescribe more effective exercise trainings.

scholarly journals The Use of Chinese Yang/Qi-Invigorating Tonic Botanical Drugs/Herbal Formulations in Ameliorating Chronic Kidney Disease by Enhancing Mitochondrial Function

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiayi Tian ◽  
Yuqi Huang ◽  
Tong Wu ◽  
Hsien-Da Huang ◽  
Kam Ming Ko ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mitochondrial Function ◽  
Antioxidant Status ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Mitochondrial Energy Metabolism ◽  
Beneficial Effects ◽  
Mitochondrial Functions ◽  
Herbal Formulations

Background: Chronic kidney disease (CKD) is a leading cause of morbidity and mortality. Mitochondrial dysfunction has been implicated as a key factor in the development of CKD. According to traditional Chinese medicine (TCM) theory, many Chinese Yang/Qi-invigorating botanical drugs/herbal formulations have been shown to produce promising outcomes in the clinical management of CKD. Experimental studies have indicated that the health-promoting action of Yang/Qi invigoration in TCM is related to the up-regulation of mitochondrial energy generation and antioxidant status.Objective: In this review, we aim to test whether Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations can provide medical benefits in CKD and its complications. And we also explore the possible involvement of mitochondrial-associated signaling pathway underlying the beneficial effects of Yang/Qi invigoration in TCM.Methods: A systematic search of “PubMed”, “China National Knowledge Infrastructure (CNKI)” and “Google Scholar” was carried out to collect all the available articles in English or Chinese related to Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations and their effects on mitochondrial function and chronic kidney disease.Result and Discussion: The relationship between the progression of CKD and mitochondrial function is discussed. The effects of Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations and their active ingredients, including phytosterols/triterpenes, flavonoids, and dibenzocyclooctadiene lignans, on CKD and related alterations in mitochondrial signaling pathways are also presented in this review. In the future, exploration of the possible beneficial effects and clinical studies of more Yang- and Qi-invigorating botanical drugs/herbal formulations in the prevention and/or/treatment of CKD and the molecular mechanisms relating to the enhancement of mitochondrial functions warrants further investigation.Conclusion: Given the critical role of mitochondrial function in safeguarding renal functional integrity, the enhancement of mitochondrial energy metabolism and antioxidant status in kidney tissue is likely involved in renal protection. Future studies on the biochemical and chemical basis underlying the effects of Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations from a mitochondrial perspective will hopefully provide novel insights into the rational development of new drugs for the prevention and/or treatment of CKD.

scholarly journals Mitochondrial DNA and Neurodegeneration: Any Role for Dietary Antioxidants?

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 764 ◽  
Author(s):  
Laura Bordoni ◽  
Rosita Gabbianelli
Keyword(s):  
Mitochondrial Function ◽  
Neurodegenerative Disorders ◽  
Neuronal Cell ◽  
Redox System ◽  
Cell Loss ◽  
Oxygen Species ◽  
Energetic Metabolism ◽  
Dietary Antioxidants ◽  
Beneficial Effects ◽  
Mitochondrial Functions

The maintenance of the mitochondrial function is essential in preventing and counteracting neurodegeneration. In particular, mitochondria of neuronal cells play a pivotal role in sustaining the high energetic metabolism of these cells and are especially prone to oxidative damage. Since overproduction of reactive oxygen species (ROS) is involved in the pathogenesis of neurodegeneration, dietary antioxidants have been suggested to counteract the detrimental effects of ROS and to preserve the mitochondrial function, thus slowing the progression and limiting the extent of neuronal cell loss in neurodegenerative disorders. In addition to their role in the redox-system homeostasis, mitochondria are unique organelles in that they contain their own genome (mtDNA), which acts at the interface between environmental exposures and the molecular triggers of neurodegeneration. Indeed, it has been demonstrated that mtDNA (including both genetics and, from recent evidence, epigenetics) might play relevant roles in modulating the risk for neurodegenerative disorders. This mini-review describes the link between the mitochondrial genome and cellular oxidative status, with a particular focus on neurodegeneration; moreover, it provides an overview on potential beneficial effects of antioxidants in preserving mitochondrial functions through the protection of mtDNA.

Dietary Polyphenols and Mitochondrial Function: Role in Health and Disease

2019 ◽  
Vol 26 (19) ◽  
pp. 3376-3406 ◽  
Author(s):  
José Teixeira ◽  
Daniel Chavarria ◽  
Fernanda Borges ◽  
Lech Wojtczak ◽  
Mariusz R. Wieckowski ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Redox Status ◽  
Dietary Polyphenols ◽  
Beneficial Effects ◽  
Regulatory Processes ◽  
In Vivo Experiments ◽  
Mitochondrial Functions ◽  
Huge Impact

Mitochondria are cytoplasmic double-membraned organelles that are involved in a myriad of key cellular regulatory processes. The loss of mitochondrial function is related to the pathogenesis of several human diseases. Over the last decades, an increasing number of studies have shown that dietary polyphenols can regulate mitochondrial redox status, and in some cases, prevent or delay disease progression. This paper aims to review the role of four dietary polyphenols – resveratrol, curcumin, epigallocatechin-3-gallate nd quercetin – in molecular pathways regulated by mitochondria and their potential impact on human health. Cumulative evidence showed that the aforementioned polyphenols improve mitochondrial functions in different in vitro and in vivo experiments. The mechanisms underlying the polyphenols’ beneficial effects include, among others, the attenuation of oxidative stress, the regulation of mitochondrial metabolism and biogenesis and the modulation of cell-death signaling cascades, among other mitochondrial-independent effects. The understanding of the chemicalbiological interactions of dietary polyphenols, namely with mitochondria, may have a huge impact on the treatment of mitochondrial dysfunction-related disorders.

scholarly journals Endoplasmic Reticulum Associated Degradation (ERAD) Deficiency Promotes Mitochondrial Dysfunction and Transcriptional Rewiring in Human Hepatic Cells

2020 ◽  
Author(s):  
Xiaoqing Yang ◽  
Qingqing Liu ◽  
Guangyu Long ◽  
Yabin Hu ◽  
Zhenglong Gu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Mammalian Cells ◽  
Structural Integrity ◽  
Protein Quality ◽  
Critical Role ◽  
Mitochondrial Outer Membrane ◽  
Genetic Ablation ◽  
Mitochondrial Functions ◽  
Quality Control Process

AbstractMitochondrial dysfunction has been associated with a variety of human diseases including neurodegeneration, diabetes, non-alcohol fatty liver disease (NAFLD) and cancer, but its underlying causes are incompletely understood. Endoplasmic reticular associated degradation (ERAD) is a protein quality control process essential for maintaining ER homeostasis. Using the human hepatic cell line HepG2 as a model, we show here that ERAD is critically required for mitochondrial function in mammalian cells. Pharmacological inhibition or genetic ablation of ERAD increases cell death under both basal conditions and in response to proinflammatory cytokines. Decreased viability of ERAD-deficient HepG2 cells was traced to impaired mitochondrial functions including reduced ATP production, enhanced reactive oxygen species (ROS) accumulation and increased mitochondrial outer membrane permeability (MOMP). Transcriptome profiling reveals widespread down-regulation in the expression of genes underpinning mitochondrial functions, and up-regulation in the genes with association to tumor growth and aggression. These results highlight a critical role for ERAD in maintaining mitochondrial functional and structural integrity and raise the possibility to improve cellular and organismal mitochondrial function via enhancing cellular ERAD capacity.

scholarly journals ERAD deficiency promotes mitochondrial dysfunction and transcriptional rewiring in human hepatic cells

2020 ◽  
Vol 295 (49) ◽  
pp. 16743-16753
Author(s):  
Qingqing Liu ◽  
Xiaoqin Yang ◽  
Guangyu Long ◽  
Yabing Hu ◽  
Zhenglong Gu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Mammalian Cells ◽  
Structural Integrity ◽  
Protein Quality ◽  
Critical Role ◽  
Mitochondrial Outer Membrane ◽  
Genetic Ablation ◽  
Mitochondrial Functions ◽  
Quality Control Process

Mitochondrial dysfunction is associated with a variety of human diseases including neurodegeneration, diabetes, nonalcohol fatty liver disease (NAFLD), and cancer, but its underlying causes are incompletely understood. Using the human hepatic cell line HepG2 as a model, we show here that endoplasmic reticulum-associated degradation (ERAD), an ER protein quality control process, is critically required for mitochondrial function in mammalian cells. Pharmacological inhibition or genetic ablation of key proteins involved in ERAD increased cell death under both basal conditions and in response to proinflammatory cytokines, a situation frequently found in NAFLD. Decreased viability of ERAD-deficient HepG2 cells was traced to impaired mitochondrial functions including reduced ATP production, enhanced reactive oxygen species (ROS) accumulation, and increased mitochondrial outer membrane permeability. Transcriptome profiling revealed widespread down-regulation of genes underpinning mitochondrial functions, and up-regulation of genes associated with tumor growth and aggression. These results highlight a critical role for ERAD in maintaining mitochondrial functional and structural integrity and raise the possibility of improving cellular and organismal mitochondrial function via enhancing cellular ERAD capacity.

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

Relation between cognitive disorders and type of physical activity: Results of the FréLE cohort

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
C Dupré ◽  
N Barth ◽  
A El Moutawakkil ◽  
F Béland ◽  
F Roche ◽  
...  
Keyword(s):  
Physical Activity ◽  
Cognitive Decline ◽  
Proportional Hazards ◽  
Cognitive Disorders ◽  
The Elderly ◽  
Cognitive Status ◽  
Global Test ◽  
Professional Activities ◽  
Beneficial Effects ◽  
The Impact

Abstract Background Few previous cohorts have studied the different type of physical activities and the degree of cognitive decline. The objective of this work was to analyze the leisure, domestic and professional activities with mild and moderate cognitive disorders in older people living in community. Methods The study used data from the longitudinal and observational study, FrèLE (FRagility: Longitudinal Study of Expressions). The collected data included: socio-demographic variables, lifestyle, and health status (frailty, comorbidities, cognitive status, depression). Cognitive decline was assessed by using: MMSE (Mini-Mental State Examination) and MoCA (Montreal Cognitive Assessment). MoCA was used with two cut-offs (26 and 17) so as to define mild and moderate cognitive disorders Physical activity was assessed by the PASE (Physical Activity Scale for the Elderly), structured in three sections: leisure, domestic and professional activities. Spline and proportional hazards regression models (Cox) were used to estimate the risk of cognitive disorders. Results At baseline, 1623 participants were included and the prevalence of cognitive disorders was 6.9% (MMSE) and 7.2% (MoCA), mild cognitive disorders was 71.3%. The mean age was 77 years, and 52% of the participants were women. After a 2 years long follow-up, we found 6.9% (MMSE) and 6% (MoCA) cognitive disorders on participants. Analyses showed that domestic activities were associated to cognitive decline (HR = 0.52 [0.28-0.94] for MMSE and HR = 0.48 [0.28-0.80] for MoCA). No association were found with leisure and professional activities, and no spline were significant with mild cognitive disorders. Conclusions Analysis showed a relationship between cognitive disorders and type of physical activity, thanks to the use of specific questionnaire of elderly and two global test of cognition. These findings will contribute to the debate on the beneficial effects of physical activity on cognition. Key messages This work allowed to compare two test of cognition and their link with physical activity. It contributes to the debate on the beneficial effects of physical activity on cognition. The work allowed us to see the effect of the different types of physical activity and the impact of the statistical method on the results.

scholarly journals Impact of SGLT2 Inhibitors on Heart Failure: From Pathophysiology to Clinical Effects

2021 ◽  
Vol 22 (11) ◽  
pp. 5863
Author(s):  
Giuseppe Palmiero ◽  
Arturo Cesaro ◽  
Erica Vetrano ◽  
Pia Clara Pafundi ◽  
Raffaele Galiero ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucose Transporter ◽  
The Elderly ◽  
Intracellular Sodium ◽  
Clinical Effects ◽  
Glucose Lowering ◽  
Beneficial Effects ◽  
Glucose Transporter 2 ◽  
Function Impairment

Heart failure (HF) affects up to over 20% of patients with type 2 diabetes (T2DM), even more in the elderly. Although, in T2DM, both hyperglycemia and the proinflammatory status induced by insulin resistance are crucial in cardiac function impairment, SGLT2i cardioprotective mechanisms against HF are several. In particular, these beneficial effects seem attributable to the significant reduction of intracellular sodium levels, well-known to exert a cardioprotective role in the prevention of oxidative stress and consequent cardiomyocyte death. From a molecular perspective, patients’ exposure to gliflozins’ treatment mimics nutrient and oxygen deprivation, with consequent autophagy stimulation. This allows to maintain the cellular homeostasis through different degradative pathways. Thus, since their introduction in the clinical practice, the hypotheses on SGLT2i mechanisms of action have changed: from simple glycosuric drugs, with consequent glucose lowering, erythropoiesis enhancing and ketogenesis stimulating, to intracellular sodium-lowering molecules. This provides their consequent cardioprotective effect, which justifies its significant reduction in CV events, especially in populations at higher risk. Finally, the updated clinical evidence of SGLT2i benefits on HF was summarized. Thus, this review aimed to analyze the cardioprotective mechanisms of sodium glucose transporter 2 inhibitors (SGLT2i) in patients with HF, as well as their clinical impact on cardiovascular events.

scholarly journals From Exercise to Cognitive Performance: Role of Irisin

2021 ◽  
Vol 11 (15) ◽  
pp. 7120
Author(s):  
Mirko Pesce ◽  
Irene La Fratta ◽  
Teresa Paolucci ◽  
Alfredo Grilli ◽  
Antonia Patruno ◽  
...  
Keyword(s):  
The Elderly ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Beneficial Effects ◽  
General Exercise ◽  
Fibronectin Type Iii ◽  
Exercise Induced ◽  
Fibronectin Type Iii Domain ◽  
The Brain

The beneficial effects of exercise on the brain are well known. In general, exercise offers an effective way to improve cognitive function in all ages, particularly in the elderly, who are considered the most vulnerable to neurodegenerative disorders. In this regard, myokines, hormones secreted by muscle in response to exercise, have recently gained attention as beneficial mediators. Irisin is a novel exercise-induced myokine, that modulates several bodily processes, such as glucose homeostasis, and reduces systemic inflammation. Irisin is cleaved from fibronectin type III domain containing 5 (FNDC5), a transmembrane precursor protein expressed in muscle under the control of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). The FNDC5/irisin system is also expressed in the hippocampus, where it stimulates the expression of the neurotrophin brain-derived neurotrophic factor in this area that is associated with learning and memory. In this review, we aimed to discuss the role of irisin as a key mediator of the beneficial effects of exercise on synaptic plasticity and memory in the elderly, suggesting its roles within the main promoters of the beneficial effects of exercise on the brain.

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