Browsing by Subject "Mitochondrial dysfunction"

Now showing 1 - 3 of 3
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    Iron in the migraine brain
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Tepe, Nermin; Yemisci, Muge; Karatas, Hulya
    Iron, a vital element for numerous peripheral and central nervous system functions, is a key player in DNA synthesis, gene expression, myelination, neurotransmission, and mitochondrial electron transport. Iron has utmost importance in various neurological functions, including neurotransmitter synthesis and brain cell metabolism. Migraine is a neurogliovascular disorder in which neuroinflammation plays a crucial role. Iron deficiency has been associated with various neurological issues and could potentially influence migraine frequency or severity. However, the relationship between iron levels and migraine is not fully clear and necessitates further research. On the other hand, iron overload could also have negative effects, as excessive iron might contribute to oxidative stress and inflammation, which may impact migraine-related pathways. The interplay between iron levels and neuroinflammation might affect migraines. While iron deficiency could exacerbate inflammation or disrupt neurotransmitter balance, iron overload might increase oxidative stress and neuroinflammation. Comprehending this balance is fundamental, as both iron deficiency and overload can have detrimental effects on brain health and migraine symptoms. In this review, we will summarize the current interconnection between migraine, iron levels, and neuroinflammation that are currently under active investigation
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    Mdivi-1: a promising drug and its underlying mechanisms in the treatment of neurodegenerative diseases
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Liu, Xiaoqin; Song, Lijuan; Yu, Jiezhong; Huang, Fang; Li, Yanhua; Ma, Cungen
    Mitochondria are energy-producing organelles, and neurons are high energy consumption cells. Therefore, mitochondrial dysfunction is a critical factor in neurodegenerative processes. Mitochondrial division inhibitor-1 (Mdivi-1) is a small chemical inhibitor of mitochondrial division dynamin, which plays multiple roles in mitochondrial dynamics, mitochondrial autophagy, ATP production, the immune response, and Ca2+ homeostasis. Mdivi-1 inhibition of excessive mitochondrial fission exerted cytoprotective effects in neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Mdivi-1 changed the mRNA expression of the electron transport chain (ETC) and reduced Ca2+ overload against neuronal injury. Elucidation of the molecular mechanism of Mdivi-1 in neurodegenerative diseases will help evaluate its therapeutic potential and promote its application in clinical studies. The present article focused on the multiple effects of Mdivi-1 on mitochondrial function and its potential therapeutic effects in neurodegenerative diseases.
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    NRIP1 is a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Zhang, Wanliu; Lu, Jingqian; Gao, Yan; Song, Qianhong; Luo, Shihua; Li, Yi
    Background and objective. From a clinical standpoint, myocardial ischemia/reperfusion injury (MIRI) has always been an enormous challenge for the treatment of acute myocardial infarction (AMI). Molecular targeting therapy may help overcome this challenge. The present work aimed to elucidate the possible involvement of Yin-Yang 1 (YY1)/nuclear receptor-interacting protein 1 (NRIP1) and discover the molecular mechanism of MIRI. Methods. Herein, a cardiomyocyte ischemia/ reperfusion (I/R) model was established via oxygen-glucose deprivation/re-oxygenation (OGD/R) damage in H9c2 cardiomyocytes. Reverse transcription-quantitative PCR and western blotting were conducted to measure the levels of YY1 and NRIP1 at the RNA and protein levels, respectively. H9c2 cell viability and apoptosis were assayed using the Cell Counting Kit-8, flow cytometry, and western blotting. In addition, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels were analyzed as markers of oxidative stress. Additionally, mitochondrial membrane potential, which was measured via JC-1 staining, ATP content, Complex I activity, mitochondrial DNA copy number, and mitochondrial permeability transition pore (mPTP) opening rate were analyzed to evaluate mitochondrial activity. Moreover, luciferase reporter and chromatin immunoprecipitation assays experimentally validated the predicted affinity of YY1 with the NRIP1 promoter according to the HumanTFDB online tool. Results. YY1/NRIP1 were both highly expressed in OGD/R-injured H9c2 cardiomyocytes. Downregulation of NRIP1 improved cell viability, whereas it inhibited cell apoptosis and oxidative stress, and suppressed mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes. Importantly, it was verified that YY1 could bind to the NRIP1 promoter to positively regulate NRIP1 expression. The protective effects of NRIP1 knockdown against cardiomyocyte damage and mitochondrial dysfunction in OGD/R-injured H9c2 cardiomyocytes were partly abolished through overexpression of YY1. Conclusion. NRIP1 emerged as a downstream target of YY1 in promoting OGD/R-induced H9c2 cardio-myocyte injury and mitochondrial dysfunction, providing novel ideas for targeted treatments to alleviate MIRI.