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

Free radicals and their impact on health and antioxidant defenses: a review DOI Creative Commons

Nisansala Chandimali,

Seon Gyeong Bak,

Eun Hyun Park

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Jan. 24, 2025

Abstract Free radicals, characterized by the presence of unpaired electrons, are highly reactive species that play a significant role in human health. These molecules can be generated through various endogenous processes, such as mitochondrial respiration and immune cell activation, well exogenous sources, including radiation, pollution, smoking. While free radicals essential for certain physiological signaling defense, their overproduction disrupt delicate balance between oxidants antioxidants, leading to oxidative stress. Oxidative stress results damage critical biomolecules like DNA, proteins, lipids, contributing pathogenesis diseases. Chronic conditions cancer, cardiovascular diseases, neurodegenerative disorders, inflammatory diseases have been strongly associated with harmful effects radicals. This review provides comprehensive overview characteristics types mechanisms formation, biological impacts. Additionally, we explore natural compounds extracts studied antioxidant properties, offering potential therapeutic avenues managing radical-induced damage. Future research directions also discussed advance our understanding treatment radical-associated

Language: Английский

Citations

8

Dysfunctional Glucose Metabolism in Alzheimer’s Disease Onset and Potential Pharmacological Interventions DOI Open Access
Vijay Kumar, So-Hyeon Kim, Kausik Bishayee

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(17), P. 9540 - 9540

Published: Aug. 23, 2022

Alzheimer’s disease (AD) is the most common age-related dementia. The alteration in metabolic characteristics determines prognosis. Patients at risk show reduced glucose uptake brain. Additionally, type 2 diabetes mellitus increases of AD with increasing age. Therefore, changes cerebral cortex may predict histopathological diagnosis AD. shifts and metabolism, insulin resistance, oxidative stress, abnormal autophagy advance pathogenesis syndrome. Here, we summarize role altered metabolism for discuss potential pharmacological interventions defects to encourage development novel therapeutic methods.

Language: Английский

Citations

60

Integrated multi-omics analysis of Alzheimer’s disease shows molecular signatures associated with disease progression and potential therapeutic targets DOI Creative Commons
Pradeep Kodam,

R. Sai Swaroop,

Sai Sanwid Pradhan

et al.

Scientific Reports, Journal Year: 2023, Volume and Issue: 13(1)

Published: March 6, 2023

Alzheimer's disease (AD) is a progressive neurodegenerative characterized by the formation of amyloid plaques implicated in neuronal death. Genetics, age, and sex are risk factors attributed to AD. Though omics studies have helped identify pathways associated with AD, an integrated systems analysis available data could help understand mechanisms, potential biomarkers, therapeutic targets. Analysis transcriptomic sets from GEO database, proteomic metabolomic literature was performed deregulated commonality identified overlapping among sets. The included those neurotransmitter synapses, oxidative stress, inflammation, vitamins, complement, coagulation pathways. Cell type showed microglia, endothelial, myeloid, lymphoid cells affected. Microglia inflammation pruning synapses implications for memory cognition. protein-cofactor network B2, B6, pantothenate shows metabolic modulated these vitamins which overlap multi-omics analysis. Overall, molecular signature Treatment anti-oxidants, genetically susceptible individuals pre-symptomatic stage might better management disease.

Language: Английский

Citations

39

Astragalin ameliorates renal injury in diabetic mice by modulating mitochondrial quality control via AMPK-dependent PGC1α pathway DOI

Mengyao Sun,

Hui-jing Ye,

Zheng Chen

et al.

Acta Pharmacologica Sinica, Journal Year: 2023, Volume and Issue: 44(8), P. 1676 - 1686

Published: March 1, 2023

Language: Английский

Citations

27

The anti-aging mechanism of ginsenosides with medicine and food homology DOI
Tiantian Tian,

Chung-Nga Ko,

Wenya Luo

et al.

Food & Function, Journal Year: 2023, Volume and Issue: 14(20), P. 9123 - 9136

Published: Jan. 1, 2023

Ginsenosides resist the aging by regulating multiple signaling pathways.

Language: Английский

Citations

24

Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review) DOI Creative Commons
Pei Qin,

Ye Sun,

Liya Li

et al.

International Journal of Molecular Medicine, Journal Year: 2024, Volume and Issue: 53(5)

Published: April 2, 2024

Chronic neuroinflammation serves a key role in the onset and progression of neurodegenerative disorders. Mitochondria serve as central regulators neuroinflammation. In addition to providing energy cells, mitochondria also participate immunoinflammatory response disorders including Alzheimer's disease, Parkinson's multiple sclerosis epilepsy, by regulating processes such cell death inflammasome activation. Under inflammatory conditions, mitochondrial oxidative stress, epigenetics, dynamics calcium homeostasis imbalance may underlying regulatory mechanisms for these diseases. Therefore, investigating related dysfunction result therapeutic strategies against chronic neurodegeneration. The present review summarizes neuroinflammatory diseases current treatment approaches that target

Language: Английский

Citations

15

Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment DOI Open Access
Ewa Tywanek, Agata Michalak, Joanna Świrska

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(9), P. 4703 - 4703

Published: April 26, 2024

Autoimmune thyroid disease (AITD) is the most common organic specific illness of gland. It may manifest as overproduction or decline thyroxine and triiodothyronine. Hyperthyroidism develops due to hormones an answer presence stimulatory antibodies against TSH receptor. Hashimoto’s thyroiditis (HT) generally characterized by peroxidase thyroglobulin antibodies, with a concomitant infiltration lymphocytes in thyroid. Due progressive destruction cells, AITD can lead subclinical overt hypothyroidism. Pathophysiology extremely complicated still not fully understood, genetic, environmental epigenetic factors involved its development. increasing incidence social awareness this pathology, there urgent need expand background concerning AITD. A growing body evidence suggests possible ways treatment apart from traditional approaches. Simultaneously, role potential new biomarkers diagnosis monitoring has been highlighted recently, too. Therefore, we decided review therapeutic trends course based on pathophysiological mechanisms, mainly focusing HT. Another aim was summarize state knowledge regarding condition.

Language: Английский

Citations

13

Altered Mitochondrial Function in MASLD: Key Features and Promising Therapeutic Approaches DOI Creative Commons
Tatjana Radosavljević,

Milica Branković,

Janko Samardžić

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 906 - 906

Published: July 26, 2024

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty (NAFLD), encompasses a range of conditions from steatosis to steatohepatitis (NASH). Its prevalence, especially among patients with metabolic syndrome, highlights its growing global impact. The pathogenesis MASLD involves dysregulation, inflammation, oxidative stress, genetic factors and, notably, mitochondrial dysfunction. Recent studies underscore the critical role dysfunction in MASLD's progression. Therapeutically, enhancing function has gained interest, along lifestyle changes and pharmacological interventions targeting processes. FDA's approval resmetirom for metabolic-associated (MASH) fibrosis marks significant step. While represents progress, further research is essential understand MASLD-related fully. Innovative strategies like gene editing small-molecule modulators, alongside interventions, can potentially improve treatment. Drug repurposing new targets will advance therapy, addressing increasing burden. Therefore, this review aims provide better understanding identify more effective preventive treatment strategies.

Language: Английский

Citations

12

Role of Uremic Toxins, Oxidative Stress, and Renal Fibrosis in Chronic Kidney Disease DOI Creative Commons
Weronika Frąk, Bartłomiej Dąbek,

Marta Balcerczyk-Lis

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(6), P. 687 - 687

Published: June 3, 2024

Affecting millions of people worldwide, chronic kidney disease is a serious medical problem. It results in decrease glomerular filtration rate below 60 mL/min/1.73 m, albuminuria, abnormalities urine sediment and pathologies detected by imaging studies lasting minimum 3 months. Patients with CKD develop uremia, as result the accumulation uremic toxins body, patients can be expected to suffer from number consequences such progression renal fibrosis, development atherosclerosis or increased incidence cardiovascular events. Another key element pathogenesis oxidative stress, resulting an imbalance between production antioxidants reactive oxygen species. Oxidative stress contributes damage cellular proteins, lipids DNA increases inflammation, perpetuating dysfunction. Additionally, fibrogenesis involving fibrous tissue kidneys occurs. In our review, we also included examples forms therapy for CKD. To improve condition patients, pharmacotherapy used, described review. Among drugs that prognosis CKD, include: GLP-1 analogues, SGLT2 inhibitors, Finerenone monoclonal antibody—Canakinumab Sacubitril/Valsartan.

Language: Английский

Citations

11

The interplay between mitochondrial dysfunction and NLRP3 inflammasome in multiple sclerosis: Therapeutic implications and animal model studies DOI Open Access
Alireza Shadab,

Mohammad Abbasi‐Kolli,

Mansoore Saharkhiz

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 175, P. 116673 - 116673

Published: May 6, 2024

Multiple sclerosis (MS) is a complex autoimmune disorder that impacts the central nervous system (CNS), resulting in inflammation, demyelination, and neurodegeneration. The NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome, multiprotein of innate immune system, serves an essential role pathogenesis MS by regulating production pro-inflammatory cytokines (IL-1β & IL-18) induction pyroptotic cell death. Mitochondrial dysfunction one main potential factors can trigger NLRP3 inflammasome activation lead to inflammation axonal damage MS. This highlights importance understanding how mitochondrial dynamics modulate activity contribute inflammatory neurodegenerative features lack comprehensive urge for introduction new therapeutic strategies led us review targeting interplay between paper also evaluates natural synthetic compounds improve function and/or inhibit thereby providing neuroprotection. Moreover, it summarizes evidence from animal models demonstrate beneficial effects these on reducing Finally, this advocates deeper investigation into molecular crosstalk as means refine targets

Language: Английский

Citations

9