Inhibition of NADPH Oxidases Prevents the Development of Osteoarthritis DOI Creative Commons

Jin Han,

Donghwi Park, Ji Young Park

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(12), P. 2346 - 2346

Published: Nov. 27, 2022

Increased oxidative stress in osteoarthritis (OA) cartilage mediates catabolic signal transduction leading to extracellular matrix degradation and chondrocyte apoptosis. This study aimed explore the contribution of NADPH oxidase (NOX), a major source cellular reactive oxygen species (ROS), process chondrocytes OA. The inhibition NOX isoforms with pan-NOX inhibitor, APX-115, significantly decreased IL-1β-induced ROS production primary and, most potently, suppressed expression marker genes proteases compared other sources. Catabolic stimuli by IL-1β treatment post-traumatic OA conditions upregulated NOX2 NOX4 chondrocytes. In model, pharmacologic protected mice against modulating MMP-13 Adamts5 Mechanistically, suppresses Rac1, p38, JNK MAPK signaling consistently restores phosphorylation IL-1β-treated conclusion, prevented development attenuating restoring mitochondrial metabolism can thus be promising class drug for

Language: Английский

Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology DOI
Helmut Sies, Vsevolod V. Belousov, Navdeep S. Chandel

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2022, Volume and Issue: 23(7), P. 499 - 515

Published: Feb. 21, 2022

Language: Английский

Citations

1034
Mitochondrial Reactive Oxygen Species in Infection and Immunity DOI Creative Commons
Arunima Mukherjee, Krishna Ghosh, Sabyasachi Chakrabortty

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(6), P. 670 - 670

Published: June 8, 2024

Reactive oxygen species (ROS) contain at least one atom and or more unpaired electrons include singlet oxygen, superoxide anion radical, hydroxyl hydroperoxyl free nitrogen radicals. Intracellular ROS can be formed as a consequence of several factors, including ultra-violet (UV) radiation, electron leakage during aerobic respiration, inflammatory responses mediated by macrophages, other external stimuli stress. The enhanced production is termed oxidative stress this leads to cellular damage, such protein carbonylation, lipid peroxidation, deoxyribonucleic acid (DNA) base modifications. This damage may manifest in various pathological states, ageing, cancer, neurological diseases, metabolic disorders like diabetes. On the hand, optimum levels have been implicated regulation many important physiological processes. For example, generated mitochondria (mitochondrial mt-ROS), byproduct transport chain (ETC), participate plethora functions, which cell growth, proliferation, immune response regulation. In current review, we will focus on mechanisms mt-ROS regulate different pathways host context infection bacteria, protozoan parasites, viruses, fungi. We also discuss how these pathogens, turn, modulate evade immunity. conclude briefly giving an overview potential therapeutic approaches involving infectious diseases.

Language: Английский

Citations

18
Oxidative stress and dysregulated long noncoding RNAs in the pathogenesis of Parkinson’s disease DOI Creative Commons
Jialu Wang,

Meitong Liu,

Jiuhan Zhao

et al.

Biological Research, Journal Year: 2025, Volume and Issue: 58(1)

Published: Jan. 27, 2025

Parkinson's disease (PD) is a progressive age-related neurodegenerative whose annual incidence increasing as populations continue to age. Although its pathogenesis has not been fully elucidated, oxidative stress shown play an important role in promoting the occurrence and development of disease. Long noncoding RNAs (lncRNAs), which are more than 200 nucleotides length, also involved PD at transcriptional level via epigenetic regulation, or post-transcriptional by participating physiological processes, including aggregation α-synuclein, mitochondrial dysfunction, stress, calcium stabilization, neuroinflammation. LncRNAs correlated during processes: affects expression multiple lncRNAs, while lncRNAs regulate many genes responses. Oxidative affect other processes associated with neurodegeneration, dysfunction increased neuroinflammation that lead neuronal death. Therefore, modulating levels specific may alleviate pathological damage have neuroprotective effects. This review discusses general mechanisms mechanism underlying PD, teases out through pathogenesis, well identifies possible lncRNAs. Reviewing published studies will help us further understand process identify potential therapeutic strategies for PD.

Language: Английский

Citations

4
Sexual Dimorphism in Migraine. Focus on Mitochondria DOI
Michał Fila, Łukasz Przysło, Marcin Derwich

et al.

Current Pain and Headache Reports, Journal Year: 2025, Volume and Issue: 29(1)

Published: Jan. 6, 2025

Language: Английский

Citations

2
Reactive Oxygen Species: Role in Pathophysiology, and Mechanism of Endogenous and Dietary Antioxidants during Oxidative Stress DOI Open Access

Mohammad Mamun Sikder,

Xiaodong Li,

Steeve Akumwami

et al.

Chonnam Medical Journal, Journal Year: 2025, Volume and Issue: 61(1), P. 32 - 32

Published: Jan. 1, 2025

Redox imbalances, which result from excessive production of reactive oxygen species (ROS) or malfunctioning the antioxidant system, are source oxidative stress. ROS affects all structural and functional components cells, either directly indirectly. In addition to causing genetic abnormalities, also oxidatively modifies proteins by protein oxidation peroxidation alters lipid structure via advanced lipoxidation, decreasing function promoting damage cell death. On other hand, low levels constitute important redox-signaling molecules in various pathways that maintain cellular homeostasis regulate key transcription factors. As a result, can affect processes, such as apoptosis, migration, differentiation, proliferation. act signaling molecules, controlling normal physiological activities at level. Furthermore, there is an increasing body evidence indicating role clinical conditions. this review, we will summarize pathological processes action during

Language: Английский

Citations

2
Mechanisms and mathematical modeling of ROS production by the mitochondrial electron transport chain DOI
Sandeep Chenna, Werner J.H. Koopman, Jochen H.M. Prehn

et al.

AJP Cell Physiology, Journal Year: 2022, Volume and Issue: 323(1), P. C69 - C83

Published: May 25, 2022

Reactive oxygen species (ROS) are recognized both as damaging molecules and intracellular signaling entities. In addition to its role in ATP generation, the mitochondrial electron transport chain (ETC) constitutes a relevant source of ROS, particular during pathological conditions. Mitochondrial ROS homeostasis depends on species- site-dependent production, their bioreactivity, diffusion, scavenging. However, our quantitative understanding has thus far been hampered by technical limitations, including lack truly site- and/or ROS-specific reporter molecules. this context, use computational models is great value complement interpret empirical data, well predict variables that difficult assess experimentally. During past decades, various mechanistic ETC-mediated production have developed. Although these often-complex generated novel insights, parameterization, analysis, integration with other not straightforward. contrast, phenomenological (sometimes termed "minimal") relatively small set equations describe relationship(s) between ROS-related parameters generally aim explore system behavior generate hypotheses for experimental validation. review, we first discuss ETC-linked introduce detailed models. Next, present how bioenergetic (e.g., NADH/NAD+ ratio membrane potential) relate site-specific within ETC relationships can be used design minimal homeostasis. Finally, illustrate applied pathophysiological aspects ROS.

Language: Английский

Citations

66
Investigating the Link between Ketogenic Diet, NAFLD, Mitochondria, and Oxidative Stress: A Narrative Review DOI Creative Commons
Antonio Paoli, Giuseppe Cerullo

Antioxidants, Journal Year: 2023, Volume and Issue: 12(5), P. 1065 - 1065

Published: May 8, 2023

Together with the global rise in obesity and metabolic syndrome, prevalence of individuals who suffer from nonalcoholic fatty liver disease (NAFLD) has risen dramatically. NAFLD is currently most common chronic includes a continuum disorders initial fat accumulation to steatohepatitis (NASH), considered more severe forms, which can evolve in, cirrhosis, hepatocellular carcinoma. Common features altered lipid metabolism mainly linked mitochondrial dysfunction, which, as vicious cycle, aggravates oxidative stress promotes inflammation and, consequence, progressive death hepatocytes form NAFLD. A ketogenic diet (KD), i.e., very low carbohydrates (<30 g/die) that induces “physiological ketosis”, been demonstrated alleviate restore function. Based on this, aim present review analyze body evidence regarding potential therapeutic role KD NAFLD, focusing interplay between mitochondria liver, effects ketosis pathways, impact

Language: Английский

Citations

42
Nonalcoholic Fatty Liver Disease and Omega-3 Fatty Acids: Mechanisms and Clinical Use DOI Creative Commons
Melinda H. Spooner, Donald Β. Jump

Annual Review of Nutrition, Journal Year: 2023, Volume and Issue: 43(1), P. 199 - 223

Published: May 19, 2023

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic worldwide, particularly in obese and type 2 diabetic individuals. Currently, there are no therapies for NAFLD that have been approved by US Food Drug Administration. Herein, we examine rationale using ω3 polyunsaturated acids (PUFAs) therapy. This focus based on finding severity associated with a reduction of hepatic C20-22 PUFAs. Because PUFAs pleiotropic regulators cell function, loss has potential to significantly impact function. We describe prevalence pathophysiology as well current therapies. also present evidence from clinical preclinical studies evaluated capacity treat NAFLD. Given evidence, dietary PUFA supplementation decrease human reducing hepatosteatosis injury.

Language: Английский

Citations

28
Focusing on mitochondria in the brain: from biology to therapeutics DOI Creative Commons

Nanshan Song,

Shuyuan Mei,

Xiang-Xu Wang

et al.

Translational Neurodegeneration, Journal Year: 2024, Volume and Issue: 13(1)

Published: April 17, 2024

Abstract Mitochondria have multiple functions such as supplying energy, regulating the redox status, and producing proteins encoded by an independent genome. They are closely related to physiology pathology of many organs tissues, among which brain is particularly prominent. The demands 20% resting metabolic rate holds highly active mitochondrial activities. Considerable research shows that mitochondria function, while defects induce or exacerbate in brain. In this review, we provide comprehensive advances biology involved functions, well mitochondria-dependent cellular events pathology. Furthermore, various perspectives explored better identify roles neurological diseases neurophenotypes diseases. Finally, therapies discussed. Mitochondrial-targeting therapeutics showing great potentials treatment

Language: Английский

Citations

15
Potential role of molecular hydrogen therapy on oxidative stress and redox signaling in chronic kidney disease DOI Open Access
Cai‐Mei Zheng, Yi‐Chou Hou, Min-Tser Liao

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 176, P. 116802 - 116802

Published: May 24, 2024

Oxidative stress plays a key role in chronic kidney disease (CKD) development and progression, inducing cell damage, inflammation, fibrosis. However, effective therapeutic interventions to slow down CKD advancement are currently lacking. The multifaceted pharmacological effects of molecular hydrogen (H2) have made it promising avenue. H2 is capable capturing harmful •OH ONOO- while maintaining the crucial reactive oxygen species (ROS) involved cellular signaling. NRF2-KEAP1 system, which manages redox balance, could be used treat CKD. activates this pathway, fortifying antioxidant defenses scavenging ROS counteract oxidative stress. can improve NRF2 signaling by using Wnt/β-catenin pathway indirectly activate mitochondria. Additionally, modulates NF-κB activity regulating status, inhibiting MAPK pathways, Trx levels. Treatment with also attenuates HIF neutralizing bolstering HIF-1α function. Furthermore, affects FOXO factors enhances enzymes. Despite encouraging results bench studies, clinical trials still limited require further investigation. focus review on hydrogen's treating renal diseases, specific regulation, discusses its potential applications.

Language: Английский

Citations

11