The role of DRAM1 in mitophagy contributes to preeclampsia regulation in mice

2019 ◽  
Author(s):  
Guoqing Chen ◽  
Ying Lin ◽  
Lu Chen ◽  
Fa Zeng ◽  
Li Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Blood Lipid ◽  
Pregnancy Complication ◽  
Urine Protein ◽  
Protein Levels ◽  
High Level ◽  
And Oxidative Stress ◽  
New Onset

Abstract Background: Preeclampsia (PE) is a pregnancy complication that is diagnosed by the new onset of hypertension and proteinuria. Although the pathogenesis of PE is still not fully understood, growing evidence indicates that oxidative stress and mitochondrial dysfunction may contribute to the progression of PE. Therefore, we aimed to determine the role of mitophagy in mitochondrial dysfunction and oxidative stress in PE. Moreover, we aimed to evaluate the role of DNA damage-regulated autophagy modulator 1 (DRAM1) in the development of PE. Results: In this study, we first constructed a mouse model of PE induced by Hif-1α and found a high level of oxidative stress, apoptosis and mitochondrial dysfunction in the placentas of PE mice. Additionally, the activity of mitophagy was decreased, and the level of DRAM1 was significantly decreased in the placentas of PE mice. To further explore the role of DRAM1 in mitophagy, DRAM1 was overexpressed in the placental tissues of PE mice. It was found that the overexpression of DRAM1 effectively improved the symptoms of PE mice and that blood lipid and urine protein levels were significantly reduced. Furthermore, DRAM1 overexpression also improved mitochondrial function and reduced oxidative stress in the placentas of PE mice. In addition, it improved mitochondrial fusion and fission and enhanced mitophagy.Conclusions: our results indicate a key role of DRAM1 in mitophagy in contributing to the regulation of PE. To our knowledge, this is the first study to confirm the role of DRAM1 in PE, and the study provides a new understanding of the pathophysiological mechanisms of PE.

scholarly journals Alzheimer’s Pathogenesis and Its Link to the Mitochondrion

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
C. Simoncini ◽  
D. Orsucci ◽  
E. Caldarazzo Ienco ◽  
G. Siciliano ◽  
U. Bonuccelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cognitive Functions ◽  
Neurodegenerative Disorder ◽  
The Elderly ◽  
Mitochondria Dysfunction ◽  
Neurodegenerative Process ◽  
Mitochondrial Impairment ◽  
And Oxidative Stress

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. This neurodegenerative disorder is clinically characterized by impairment of cognitive functions and changes in behaviour and personality. The pathogenesis of AD is still unclear. Recent evidence supports some role of mitochondria dysfunction and oxidative stress in the development of the neurodegenerative process. In this review, we discuss the role of mitochondrial dysfunction in AD, focusing on the mechanisms that lead to mitochondrial impairment, oxidative stress, and neurodegeneration, a “vicious circle” that ends in dementia.

scholarly journals The role of mitochondria-targeted antioxidant MitoQ in neurodegenerative disease

2018 ◽  
pp. 1-8
Author(s):  
Linlin Zhang ◽  
Aurelio Reyes ◽  
Xiangdong Wang
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disease ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
And Oxidative Stress

Abstract: The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondriatargeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’ s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.  

scholarly journals Magnesium Lithospermate B Downregulates the Levels of Blood Pressure, Inflammation, and Oxidative Stress in Pregnant Rats with Hypertension

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Kaixiang Xu ◽  
Xiaohong Zang ◽  
Mian Peng ◽  
Qian Zhao ◽  
Binbin Lin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Gestational Hypertension ◽  
Protective Effects ◽  
Urine Protein ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Arterial Blood ◽  
Magnesium Lithospermate B ◽  
And Oxidative Stress

Background. Magnesium lithospermate B (MLB) was shown to suppress oxidative stress and reduce hypertension, but the role of MLB in pregnancy-induced hypertension (PIH) remains unknown. The objective of this study was to demonstrate the effects of MLB on rats with PIH. Methods. A total of 40 pregnant SD rats were selected, and 30 rats were orally given NG-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg/day) to establish PIH rat models. Rats were equally divided into four groups: control, PIH, 5 mg/kg MLB, and 10 mg/kg MLB. MLB was consecutively administered into PIH rats for one week. The effects of MLB on mean arterial blood pressure (MAP), urine protein level, inflammation, and oxidative stress together with angiogenesis were analyzed. Results. MLB prevented the elevation in MAP and urine protein levels induced by L-NAME. The activities of inflammatory cytokines were highly increased in serum and placental tissues of PIH rats, while cotreatment with MLB partially reversed the activities of these cytokines. MLB also recovered the expression of reactive oxygen species (ROS) in plasma of PIH rats together with levels of oxidative stress and antioxidant capacity in the placenta of PIH rats. The decreased expressions of vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and NO observed in PIH rats were increased by MLB. In addition, 10 mg/kg MLB exhibited higher protective effects as compared to lower doses of 5 mg/kg. Conclusion. This study demonstrated that pretreatment with MLB decreased MAP, inflammation, and oxidative stress in rats with gestational hypertension.

scholarly journals The perplexing pregnancy disorder preeclampsia: what next?

2018 ◽  
Vol 50 (6) ◽  
pp. 459-467 ◽  
Author(s):  
James M. Roberts
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Animal Experimentation ◽  
Placental Dysfunction ◽  
Prediction And Prevention ◽  
Inflammatory Activation ◽  
Cause Of Deaths ◽  
And Oxidative Stress ◽  
New Onset

Preeclampsia occurs in 3–5% of pregnancies and is a leading cause of deaths of mothers and their infants worldwide. It was initially described over 100 yr ago as a pregnancy abnormality defined by new-onset hypertension and proteinuria. Progress in understanding the pathophysiology was impeded by attention to these diagnostic findings. Hypertension and proteinuria were actually serendipitously recognized components of a complex multisystemic syndrome and not especially pertinent to outcome. With the recognition of inflammatory activation with consequent endothelial dysfunction 30 yr ago redirection of research resulted in an explosive increase in understanding of the disorder. The immunological origins, the role of the placenta and its functional alterations due to endoplasmic reticulum and oxidative stress, identification of placental products linking placental dysfunction to maternal systemic pathophysiology, and the role of the maternal constitution have been elegantly demonstrated by clinical, fundamental, and epidemiological findings and clever animal experimentation. Nonetheless, this increase in knowledge has not translated into improved prediction and prevention of preeclampsia. In this presentation the likelihood is discussed that this is secondary to a much greater complexity than has been previously considered and the existence of subtypes of preeclampsia that may not share an identical pathophysiology. The necessity for collaboration with data, sample, and intellectual sharing is addressed. An approach to addressing the challenges posed to such collaboration exemplified by the Global Pregnancy Collaboration is presented.

scholarly journals Oxidative Stress and Epilepsy: Literature Review

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Carlos Clayton Torres Aguiar ◽  
Anália Barbosa Almeida ◽  
Paulo Victor Pontes Araújo ◽  
Rita Neuma Dantas Cavalcante de Abreu ◽  
Edna Maria Camelo Chaves ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Mitochondrial Dysfunction ◽  
Experimental Studies ◽  
Cellular Damage ◽  
Brain Disorder ◽  
Chronic Oxidative Stress ◽  
Seizure Models ◽  
And Oxidative Stress

Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy.Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed.Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.

Protective role of amantadine in mitochondrial dysfunction and oxidative stress mediated by hepatitis C virus protein expression

2014 ◽  
Vol 89 (4) ◽  
pp. 545-556 ◽  
Author(s):  
Giovanni Quarato ◽  
Rosella Scrima ◽  
Maria Ripoli ◽  
Francesca Agriesti ◽  
Darius Moradpour ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protein Expression ◽  
Mitochondrial Dysfunction ◽  
Protective Role ◽  
Virus Protein ◽  
And Oxidative Stress

A Review on Mitochondrial Dysfunction and Oxidative stress due to Complex-Ⅰ in Parkinson Disease

2021 ◽  
pp. 167-170
Author(s):  
V Nuthan Kumar Babu ◽  
Navneet Khurana
Keyword(s):  
Oxidative Stress ◽  
Parkinson Disease ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorder ◽  
Dimethyl Fumarate ◽  
World Population ◽  
Emerging Therapies ◽  
And Oxidative Stress ◽  
Transplantation Therapy

Parkinson’s disease (PD) is the common physical movement disorder, and it is 2nd most progressive widespread neurodegenerative disorder all over the world, and it is reported that and essential 10 million, over 0.3 % of the total world population. A thoughtful reduction of the neurotransmitter dopamine (DA) in the striatum is the main cause of these motor symptoms, collectively known as parkinsonism. Mitochondria serves as most important organelle in most of the cells and are essential for life and it is also called as heart for all cellular metabolisms. The main and most important role of mitochondria is generation of ATP via oxidative phosphorylation. In this study will study about how complex Ⅰ deficiency effects the mitochondrial and oxidative stress and reactive oxygen species which cause mitochondrial dysfunction and we also study emerging therapies for Parkinson disease with the help of coenzyme Q10 and some genes like FUN-14, FUNDC-1 and dimethyl fumarate or BG-12 in some phases of clinical trials and also by cell transplantation therapy and in future this study helps in finding how this sporadic Parkinson disease occurs in parkinsonism.

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