Aging - Oxidative stress, antioxidants and computational modeling

Heliyon, Journal Year: 2020, Volume and Issue: 6(5), P. e04107 - e04107

Published: May 1, 2020

Aging is a degenerative, biological, time-dependent, universally conserved process thus designed as one of the highest known risk factors for morbidity and mortality. Every individual has its own aging mechanisms both environmental conditions (75%) genetics (25%) account aging. Several theories have been proposed until now but not even single theory solves this mystery. There are still some queries un-answered to scientific community regarding behind However, oxidative stress (OST) considered famous that sees mitochondria leading organelles which largely contribute process. Many reactive oxygen species (ROS) produced endogenously exogenously associated with But mitochondrial ROS dysfunction due contributors toward Although damage cell machinery, new evidence suggests their role in signal transduction regulate biological physiological processes. Moreover, besides mitochondria, other important such peroxisome endoplasmic reticulum also produce nature provided humans free radical scavengers called antioxidants protect from harmful effects ROS. Future predictions aging, biochemical involved, biomarkers internal external can be easily done machine learning algorithms computational models. This review explains aspects contribution producing importance fighting against ROS, different models developed understand complexities

Language: Английский

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The Good and the Bad of Mitochondrial Breakups

Trends in Cell Biology, Journal Year: 2019, Volume and Issue: 29(11), P. 888 - 900

Published: Sept. 5, 2019

Language: Английский

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The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury

Antioxidants, Journal Year: 2019, Volume and Issue: 8(10), P. 454 - 454

Published: Oct. 6, 2019

Mitochondria play a critical role in maintaining cellular function by ATP production. They are also source of reactive oxygen species (ROS) and proapoptotic factors. The mitochondria has been established many aspects cell physiology/pathophysiology, including signaling. may deteriorate under various pathological conditions, ischemia-reperfusion (IR) injury. Mitochondrial injury can be one the main causes for cardiac other tissue injuries energy stress overproduction toxic species, leading to oxidative stress, elevated calcium apoptotic necrotic death. However, interplay among these processes normal conditions is still poorly understood. IR injury, where they directly involved several pathophysiological mechanisms. We discuss context mitochondrial dynamics, specializations heterogeneity. Also, we wanted existence morphologically functionally different subpopulations heart that have sensitivities diseases Therefore, cardioprotective interventions modulate stability, dynamics turnover, pharmacologic agents, specific antioxidants uncouplers, ischemic preconditioning considered as strategies protect cardiovascular thus enhance longevity.

Language: Английский

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Obesity and aging: Molecular mechanisms and therapeutic approaches

Ageing Research Reviews, Journal Year: 2021, Volume and Issue: 67, P. 101268 - 101268

Published: Feb. 6, 2021

Language: Английский

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MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

Nature Communications, Journal Year: 2021, Volume and Issue: 12(1)

Published: Jan. 20, 2021

Abstract Healthy aging can be promoted by enhanced metabolic fitness and physical capacity. Mitochondria are chief organelles with strong implications in that also coordinate broad physiological functions, part, using peptides encoded within their independent genome. However, mitochondrial-encoded factors actively regulate unknown. Here, we report MOTS-c significantly enhance performance young (2 mo.), middle-age (12 old (22 mo.) mice. (i) nuclear genes, including those related to metabolism proteostasis, (ii) skeletal muscle metabolism, (iii) myoblast adaptation stress. We provide evidence late-life (23.5 initiated intermittent treatment (3x/week) increase capacity healthspan In humans, exercise induces endogenous expression circulation. Our data indicate is regulated genes both of our co-evolved mitochondrial genomes.

Language: Английский

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Metformin in aging and aging-related diseases: clinical applications and relevant mechanisms

Theranostics, Journal Year: 2022, Volume and Issue: 12(6), P. 2722 - 2740

Published: Jan. 1, 2022

Aging is a natural process, which plays critical role in the pathogenesis of variety diseases, i.e., aging-related such as diabetes, osteoarthritis, Alzheimer disease, cardiovascular cancers, obesity and other metabolic abnormalities.Metformin, most widely used antidiabetic drug, has been reported to delay aging display protective effect on attenuating progression various diseases by impacting key hallmark events aging, including dysregulated nutrient sensing, loss proteostasis, mitochondrial dysfunction, altered intercellular communication, telomere attrition, genomic instability, epigenetic alterations, stem cell exhaustion cellular senescence.In this review, we provide updated information knowledge applications metformin prevention treatment diseases.We focus our discussions roles underlying mechanisms modulating treating diseases.

Language: Английский

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The Key Role of Mitochondrial Function in Health and Disease

Antioxidants, Journal Year: 2023, Volume and Issue: 12(4), P. 782 - 782

Published: March 23, 2023

The role of mitochondrial function in health and disease has become increasingly recognized, particularly the last two decades. Mitochondrial dysfunction as well disruptions cellular bioenergetics have been shown to be ubiquitous some most prevalent diseases our society, such type 2 diabetes, cardiovascular disease, metabolic syndrome, cancer, Alzheimer’s disease. However, etiology pathogenesis multiple yet elucidated, making it one significant medical challenges history. rapid advances knowledge metabolism coupled with novel understanding at molecular genetic levels show tremendous promise day elucidate mysteries this ancient organelle order treat therapeutically when needed. DNA mutations, infections, aging, a lack physical activity identified major players diseases. This review examines complexities function, whose incorporation into eukaryotic cells for energy purposes was key survival creation new species. Among these complexities, tightly intertwined derived from combustion alimentary substrates oxygen are necessary homeostasis, including production reactive discusses different etiological mechanisms by which mitochondria could dysregulated, determining fate tissues organs being protagonist many non–communicable Finally, is canonical evolutionary characteristic humans that remains embedded genes. normalization modern society led perception exercise an “intervention”. modus vivendi engrained genes sedentary real intervention collateral effect societies. It known leads and, hence, probably becomes factor affecting Since only stimulus we know can improve maintain emphasis on promotion should imperative prevent populations chronic where involved, individualized prescription crucial “metabolic rehabilitation” patients. From lessons learned elite athletes (the perfect human machines), possible translate apply concepts betterment

Language: Английский

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Connecting aging biology and inflammation in the omics era

Journal of Clinical Investigation, Journal Year: 2022, Volume and Issue: 132(14)

Published: July 14, 2022

Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood solid tissues, termed inflammaging. Inflammaging has been implicated pathogenesis many age-associated chronic diseases as well loss physical cognitive function. The search for mechanisms underlie inflammaging focused initially on hallmarks aging, but it rapidly expanding multiple directions. Here, we discuss threads connecting cellular senescence mitochondrial dysfunction impaired mitophagy DNA damage, which may act hub We explore emerging multi-omics efforts aspire define complexity - identify molecular signatures novel targets interventions aimed at counteracting excessive inflammation its deleterious consequences while preserving physiological immune response. Finally, review evidence involved brain aging neurodegenerative diseases. Our goal broaden research agenda with an eye new therapeutic opportunities.

Language: Английский

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Mitochondrial DNA Release in Innate Immune Signaling

Annual Review of Biochemistry, Journal Year: 2023, Volume and Issue: 92(1), P. 299 - 332

Published: March 31, 2023

According to the endosymbiotic theory, most of DNA original bacterial endosymbiont has been lost or transferred nucleus, leaving a much smaller (∼16 kb in mammals), circular molecule that is present-day mitochondrial (mtDNA). The ability mtDNA escape mitochondria and integrate into nuclear genome was discovered budding yeast, along with genes regulate this process. Mitochondria have emerged as key regulators innate immunity, it now recognized released cytoplasm, outside cell, circulation activates multiple immune signaling pathways. Here, we first review mechanisms through which including several inducible pores defective mitophagy autophagy. Next, cover how different forms activate specific nucleic acid sensors inflammasomes. Finally, discuss intracellular extracellular release, circulating cell-free promotes systemic inflammation, are implicated human diseases, viral infections, senescence aging.

Language: Английский

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Insights from a 30-year journey: function, regulation and therapeutic modulation of PD1

Nature reviews. Immunology, Journal Year: 2023, Volume and Issue: 23(10), P. 682 - 695

Published: April 25, 2023

Language: Английский

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