Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions DOI Creative Commons
И. Ф. Беленичев, Olena Popazova, Nina Bukhtiyarova

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 108 - 108

Published: Jan. 18, 2025

The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation reactive oxygen species (ROS), calcium homeostasis, and execution apoptotic processes. Disruptions function, driven by factors such as oxidative stress, excitotoxicity, altered ion balance, lead to neuronal death contribute cognitive impairments several brain diseases. Mitochondrial can arise from genetic mutations, ischemic events, hypoxia, other environmental factors. This article highlights critical role progression diseases discusses need targeted therapeutic strategies attenuate damage, restore enhance neuroprotection.

Language: Английский

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments DOI Creative Commons
Jun Guo, Xiuqing Huang, Lin Dou

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: Dec. 16, 2022

Aging is a gradual and irreversible pathophysiological process. It presents with declines in tissue cell functions significant increases the risks of various aging-related diseases, including neurodegenerative cardiovascular metabolic musculoskeletal immune system diseases. Although development modern medicine has promoted human health greatly extended life expectancy, aging society, variety chronic diseases have gradually become most important causes disability death elderly individuals. Current research on focuses elucidating how endogenous exogenous stresses (such as genomic instability, telomere dysfunction, epigenetic alterations, loss proteostasis, compromise autophagy, mitochondrial cellular senescence, stem exhaustion, altered intercellular communication, deregulated nutrient sensing) participate regulation aging. Furthermore, thorough pathogenesis to identify interventions that promote longevity caloric restriction, microbiota transplantation, nutritional intervention) clinical treatment methods for (depletion senescent cells, therapy, antioxidative anti-inflammatory treatments, hormone replacement therapy) could decrease incidence turn healthy longevity.

Language: Английский

Citations

690

Mechanisms of Oxidative Stress in Metabolic Syndrome DOI Open Access
Sepiso K. Masenga,

Lombe S. Kabwe,

Martin Chakulya

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(9), P. 7898 - 7898

Published: April 26, 2023

Metabolic syndrome is a cluster of conditions associated with the risk diabetes mellitus type 2 and cardiovascular diseases (CVDs). closely related to obesity. Increased adiposity promotes inflammation oxidative stress, which are precursors various complications involving metabolic components, namely insulin resistance, hypertension, hyperlipidemia. An increasing number studies confirm importance stress chronic in etiology syndrome. However, few have reviewed mechanisms underlying role contributing In this review, we highlight by reactive oxygen species (ROS) increase mitochondrial dysfunction, protein damage, lipid peroxidation, impair antioxidant function Biomarkers can be used disease diagnosis evaluation severity.

Language: Английский

Citations

262

The Lactoferrin Phenomenon—A Miracle Molecule DOI Creative Commons
Paweł Kowalczyk, Katarzyna Kaczyńska, Patrycja Kleczkowska

et al.

Molecules, Journal Year: 2022, Volume and Issue: 27(9), P. 2941 - 2941

Published: May 4, 2022

Numerous harmful factors that affect the human body from birth to old age cause many disturbances, e.g., in structure of genome, inducing cell apoptosis and their degeneration, which leads development diseases, including cancer. Among leading pathological processes, microbes, viruses, gene dysregulation immune system disorders have been described. The function a protective agent may be played by lactoferrin as "miracle molecule", an endogenous protein with number favorable antimicrobial, antiviral, antioxidant, immunostimulatory binding DNA properties. purpose this article is present broad spectrum properties role plays protecting cells at all stages life.

Language: Английский

Citations

113

COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction DOI Open Access
Ekaterina Georgieva, Julian Ananiev,

Y. Yovchev

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(19), P. 14876 - 14876

Published: Oct. 4, 2023

SARS-CoV-2 infection, discovered and isolated in Wuhan City, Hubei Province, China, causes acute atypical respiratory symptoms has led to profound changes our lives. COVID-19 is characterized by a wide range of complications, which include pulmonary embolism, thromboembolism arterial clot formation, arrhythmias, cardiomyopathy, multiorgan failure, more. The disease caused worldwide pandemic, despite various measures such as social distancing, preventive strategies, therapeutic approaches, the creation vaccines, novel coronavirus infection (COVID-19) still hides many mysteries for scientific community. Oxidative stress been suggested play an essential role pathogenesis COVID-19, determining free radical levels patients with may provide insight into severity. generation abnormal oxidants under COVID-19-induced cytokine storm irreversible oxidation macromolecules subsequent damage cells, tissues, organs. Clinical studies have shown that oxidative initiates endothelial damage, increases risk complications post-COVID-19 or long-COVID-19 cases. This review describes radicals mediation mitochondrial dysfunction.

Language: Английский

Citations

58

Preclinical modeling in depression and anxiety: Current challenges and future research directions DOI Creative Commons
Masaru Tanaka, Ágnes Szabó, László Vécsei

et al.

Advances in Clinical and Experimental Medicine, Journal Year: 2023, Volume and Issue: 32(5), P. 505 - 509

Published: May 22, 2023

This editorial highlights the limitations of preclinical models in accurately reflecting complexity anxiety and depression, which leads to a lack effective treatments for these disorders. Inconsistencies experimental designs methodologies can entail conflicting or inconclusive findings, while an overreliance on medication mask underlying problems. Researchers are exploring new approaches modeling negative emotional disorders, including using patient-derived cells, developing more complex animal models, integrating genetic environmental factors. Advanced technologies, such as optogenetics, chemogenetics neuroimaging, also being employed improve specificity selectivity models. Collaboration innovation across different disciplines sectors needed address societal challenges, requires funding support that prioritize cooperation multidisciplinary research. By harnessing power technology ways working, researchers collaborate effectively bring about transformative change.

Language: Английский

Citations

50

Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation DOI Open Access
Tsung‐Hsien Chen, Hsiang‐Chen Wang, Chia-Jung Chang

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(2), P. 1314 - 1314

Published: Jan. 21, 2024

Mitochondria are critical for providing energy to maintain cell viability. Oxidative phosphorylation involves the transfer of electrons from substrates oxygen produce adenosine triphosphate. also regulate proliferation, metastasis, and deterioration. The flow in mitochondrial respiratory chain generates reactive species (ROS), which harmful cells at high levels. stress caused by ROS accumulation has been associated with an increased risk cancer, cardiovascular liver diseases. Glutathione (GSH) is abundant cellular antioxidant that primarily synthesized cytoplasm delivered mitochondria. Mitochondrial glutathione (mGSH) metabolizes hydrogen peroxide within A long-term imbalance ratio mGSH can cause dysfunction, apoptosis, necroptosis, ferroptosis, may lead disease. This study aimed review physiological functions, anabolism, variations organ tissue accumulation, delivery GSH mitochondria relationships between levels, GSH/GSH disulfide (GSSG) ratio, programmed death, ferroptosis. We discuss diseases deficiency related therapeutics.

Language: Английский

Citations

48

Kaempferol: Paving the path for advanced treatments in aging-related diseases DOI Creative Commons
Md Sadique Hussain, Abdulmalik Saleh Alfawaz Altamimi, Muhammad Afzal

et al.

Experimental Gerontology, Journal Year: 2024, Volume and Issue: 188, P. 112389 - 112389

Published: March 8, 2024

Aging-related diseases (ARDs) are a major global health concern, and the development of effective therapies is urgently needed. Kaempferol, flavonoid found in several plants, has emerged as promising candidate for ameliorating ARDs. This comprehensive review examines Kaempferol's chemical properties, safety profile, pharmacokinetics, highlights its potential therapeutic utility against underpinned by distinctive structure, which confers antioxidative anti-inflammatory properties. Kaempferol counteracts reactive oxygen species (ROS) modulates crucial cellular pathways, thereby combating oxidative stress inflammation, hallmarks low toxicity wide margins, demonstrated preclinical clinical studies, further substantiate potential. Compelling evidence supports substantial addressing ARDs through mechanisms, notably anti-inflammatory, antioxidant, anti-apoptotic actions. exhibits versatile neuroprotective effect modulating various proinflammatory signaling including NF-kB, p38MAPK, AKT, β-catenin cascade. Additionally, it hinders formation aggregation beta-amyloid protein regulates brain-derived neurotrophic factors. In terms anticancer potential, kaempferol acts diverse inducing apoptosis, arresting cell cycle at G2/M phase, suppressing epithelial-mesenchymal transition (EMT)-related markers, affecting phosphoinositide 3-kinase/protein kinase B pathways. Subsequent studies should focus on refining dosage regimens, exploring innovative delivery systems, conducting trials to translate these findings into applications.

Language: Английский

Citations

48

Polycystic Ovary Syndrome and Oxidative Stress—From Bench to Bedside DOI Open Access
Natalia Żeber‐Lubecka, Michał Ciebiera, Ewa E. Hennig

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(18), P. 14126 - 14126

Published: Sept. 15, 2023

Oxidative stress (OS) is a condition that occurs as result of an imbalance between the production reactive oxygen species (ROS) and body's ability to detoxify neutralize them. It can play role in variety reproductive system conditions, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia, infertility. In this review, we briefly discuss links oxidative PCOS. Mitochondrial mutations may lead impaired phosphorylation (OXPHOS), decreased adenosine triphosphate (ATP) production, increased ROS. These functional consequences contribute metabolic hormonal dysregulation observed Studies have shown OS negatively affects ovarian follicles disrupts normal follicular development maturation. Excessive ROS damage oocytes granulosa cells within follicles, impairing their quality compromising fertility. Impaired OXPHOS mitochondrial dysfunction insulin resistance (IR) by disrupting signaling pathways glucose metabolism. Due dysfunctional OXPHOS, reduced ATP hinder insulin-stimulated uptake, leading IR. Hyperandrogenism promotes inflammation IR, both which increase OS. A detrimental feedback loop ensues IR escalates, causing elevated levels exacerbate Exploring relations PCOS crucial fully understand pathophysiology develop effective treatment strategies improve life women affected condition. The antioxidants potential therapies also discussed.

Language: Английский

Citations

44

New insights into the role of mitochondrial dynamics in oxidative stress-induced diseases DOI Open Access
Sisi Chen, Qilong Li,

Hanjing Shi

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 178, P. 117084 - 117084

Published: Aug. 1, 2024

The accumulation of excess reactive oxygen species (ROS) can lead to oxidative stress (OS), which induce gene mutations, protein denaturation, and lipid peroxidation directly or indirectly. expression is reduced ATP level in cells, increased cytoplasmic Ca

Language: Английский

Citations

41

Expanding the Frontiers of Guardian Antioxidant Selenoproteins in Cardiovascular Pathophysiology DOI
Tommaso Angelone, Carmine Rocca, Vincenzo Lionetti

et al.

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: 40(7-9), P. 369 - 432

Published: Feb. 1, 2024

Physiological levels of reactive oxygen and nitrogen species (ROS/RNS) function as fundamental messengers for many cellular developmental processes in the cardiovascular system. ROS/RNS involved cardiac redox-signaling originate from diverse sources, their are tightly controlled by key endogenous antioxidant systems that counteract accumulation. However, dysregulated redox-stress resulting inefficient removal leads to inflammation, mitochondrial dysfunction, cell death, contributing development progression disease (CVD).

Language: Английский

Citations

18