scholarly journals Autophagy and the Lysosomal System in Cancer

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2752
Author(s):  
Suresh Kumar ◽  
Miguel Sánchez-Álvarez ◽  
Fidel-Nicolás Lolo ◽  
Flavia Trionfetti ◽  
Raffaele Strippoli ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Current Knowledge ◽  
Transcriptional Regulator ◽  
Therapeutic Interventions ◽  
Control Network ◽  
Ros Production ◽  
Oxygen Species ◽  
Lysosomal System ◽  
Key Aspects ◽  
And Control

Autophagy and the lysosomal system, together referred to as the autophagolysosomal system, is a cellular quality control network which maintains cellular health and homeostasis by removing cellular waste including protein aggregates, damaged organelles, and invading pathogens. As such, the autophagolysosomal system has roles in a variety of pathophysiological disorders, including cancer, neurological disorders, immune- and inflammation-related diseases, and metabolic alterations, among others. The autophagolysosomal system is controlled by TFEB, a master transcriptional regulator driving the expression of multiple genes, including autophagoly sosomal components. Importantly, Reactive Oxygen Species (ROS) production and control are key aspects of the physiopathological roles of the autophagolysosomal system, and may hold a key for synergistic therapeutic interventions. In this study, we reviewed our current knowledge on the biology and physiopathology of the autophagolysosomal system, and its potential for therapeutic intervention in cancer.

Toxocariasis. Difficult diagnosis in practice of pediatrician

2021 ◽  
pp. 37-41
Author(s):  
K. D. Ermolenko
Keyword(s):  
Neurological Disorders ◽  
Web Of Science ◽  
Oral Route ◽  
Parasitic Nematodes ◽  
Clinical Center ◽  
Key Aspects ◽  
And Control ◽  
The Impact ◽  
The Relationship ◽  
Epidemiological Information

Parasitic nematodes of the genus Toxocara are socio-economically important zoonotic pathogens. These parasites are usually directly transmitted to the human host through the fecal-oral route and can cause toxocariasis and related complications, including allergic and neurological disorders. Although tens of millions of people are estimated to have been exposed to Toxocara spp. or are infected with them, global epidemiological information on the relationship between seropositivity and toxocariasis is limited. Recent results show that in some countries the impact of toxocariasis on human health is increasing. The purpose of this review was to analyze modern data on the epidemiology, pathogenesis, clinical and laboratory manifestations and therapy of toxocariasis. Material and methods. The analysis of publications in PubMed, EMBASE and Web of Science systems in the period from January 1950 to September 2020, highlighting studies documenting the epidemiological, pathogenetic, clinical and laboratory aspects of toxocariasis. In addition, we analyzed clinical cases of toxocariasis among patients of the departments of the Pediatric Research and Clinical Center for Infectious Diseases. The article discusses the basic information about toxocars, summarizes the key aspects of the pathogenesis, diagnosis and treatment of toxocariasis, its prevalence, and gives recommendations for the prevention and control of this disease.

scholarly journals Oxidative Stress Contributes to Endothelial Dysfunction in Mouse Models of Hereditary Hemorrhagic Telangiectasia

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Mirjana Jerkic ◽  
Valentin Sotov ◽  
Michelle Letarte
Keyword(s):  
Endothelial Dysfunction ◽  
Hereditary Hemorrhagic Telangiectasia ◽  
Transforming Growth Factor ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Enos Uncoupling ◽  
Receptor Like Kinase ◽  
Vascular Dysplasia ◽  
And Control

Hereditary hemorrhagic telangiectasia (HHT) is a vascular dysplasia caused by mutations in endoglin (ENG; HHT1) or activin receptor-like kinase (ALK1; HHT2) genes, coding for transforming growth factor-β(TGF-β) superfamily receptors. We demonstrated previously that endoglin and ALK1 interact with endothelial NO synthase (eNOS) and affect its activation. Endothelial cells deficient in endoglin or ALK1 proteins show eNOS uncoupling, reduced NO, and increased reactive oxygen species (ROS) production. In this study, we measured NO and H2O2levels in several organs of adultEngandAlk1heterozygous mice, to ascertain whether decreased NO and increased ROS production is a generalized manifestation of HHT. A significant reduction in NO and increase in ROS production were found in several organs, known to be affected in patients. ROS overproduction in mutant mice was attributed to eNOS, as it was L-NAME inhibitable. Mitochondrial ROS contribution, blocked by antimycin, was highest in liver while NADPH oxidase, inhibited by apocynin, was a major source of ROS in the other tissues. However, there was no difference in antimycin- and apocynin-inhibitable ROS production between mutant and control mice. Our results indicate that eNOS-derived ROS contributes to endothelial dysfunction and likely predisposes to disease manifestations in several organs of HHT patients.

scholarly journals ANTIMICROBIAL RESISTANCE OF ESCHERIСHIA COLI STRAINS ISOLATED FROM PATIENTS WITH PURULENT PERITONITIS

2021 ◽  
pp. 53-57
Author(s):  
O. V. Kotsar ◽  
O. V. Kochnieva
Keyword(s):  
Bacterial Infections ◽  
Current Knowledge ◽  
Abdominal Cavity ◽  
Multidrug Resistant ◽  
Therapeutic Interventions ◽  
Health Concern ◽  
Promising Alternative ◽  
E Coli ◽  
Purulent Peritonitis ◽  
And Control

Escherichia coli remains one of the most frequent causes of several common bacterial infections in humans. Surgery on the abdominal cavity is usually complicated by peritonitis caused by E. coli strains. Recently, there are data confirming the high degree of resistance of this strain. The prevalence of multidrug-resistant E. coli strains is increasing worldwide principally due to the spread of mobile genetic elements, such as plasmids. The rise of multidrug-resistant strains of E. coli also occurs in Ukraine. Therefore, the spread of resistance E. coli is an increasing public health concern in our country. This paper summarizes the antibiotic resistance of clinical E. coli strains, isolated from patients with peritonitis. Furthermore, therapeutic interventions and strategies to prevent and control infections are presented and discussed. The article also provides an overview of the current knowledge concerning promising alternative therapies against E. coli diseases.

scholarly journals Cross-talk between redox signalling and protein aggregation

2020 ◽  
Vol 48 (2) ◽  
pp. 379-397 ◽  
Author(s):  
Loes van Dam ◽  
Tobias B. Dansen
Keyword(s):  
Reactive Oxygen Species ◽  
Stress Response ◽  
Protein Aggregation ◽  
Cross Talk ◽  
Current Knowledge ◽  
Causal Relation ◽  
Amyloid Formation ◽  
Ros Production ◽  
Oxygen Species ◽  
Redox Signalling

It is well established that both an increase in reactive oxygen species (ROS: i.e. O2•−, H2O2 and OH•), as well as protein aggregation, accompany ageing and proteinopathies such as Parkinson's and Alzheimer's disease. However, it is far from clear whether there is a causal relation between the two. This review describes how protein aggregation can be affected both by redox signalling (downstream of H2O2), as well as by ROS-induced damage, and aims to give an overview of the current knowledge of how redox signalling affects protein aggregation and vice versa. Redox signalling has been shown to play roles in almost every step of protein aggregation and amyloid formation, from aggregation initiation to the rapid oligomerization of large amyloids, which tend to be less toxic than oligomeric prefibrillar aggregates. We explore the hypothesis that age-associated elevated ROS production could be part of a redox signalling-dependent-stress response in an attempt to curb protein aggregation and minimize toxicity.

New roles for old pathways? A circuitous relationship between reactive oxygen species and cyclo-oxygenase in hypertension

2013 ◽  
Vol 126 (2) ◽  
pp. 111-121 ◽  
Author(s):  
Raquel Hernanz ◽  
Ana M. Briones ◽  
Mercedes Salaices ◽  
María J. Alonso
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Function ◽  
Current Knowledge ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Prostaglandin Synthase ◽  
New Findings ◽  
Hypertension Development

Elevated production of prostanoids from the constitutive (COX-1) or inducible (COX-2) cyclo-oxygenases has been involved in the alterations in vascular function, structure and mechanical properties observed in cardiovascular diseases, including hypertension. In addition, it is well known that production of ROS (reactive oxygen species) plays an important role in the impaired contractile and vasodilator responses, vascular remodelling and altered vascular mechanics of hypertension. Of particular interest is the cross-talk between NADPH oxidase and mitochondria, the main ROS sources in hypertension, which may represent a vicious feed-forward cycle of ROS production. In recent years, there is experimental evidence showing a relationship between ROS and COX-derived products. Thus ROS can activate COX and the COX/PG (prostaglandin) synthase pathways can induce ROS production through effects on different ROS generating enzymes. Additionally, recent evidence suggests that the COX–ROS axis might constitute a vicious circle of self-perpetuating vasoactive products that have a pathophysiological role in altered vascular contractile and dilator responses and hypertension development. The present review discusses the current knowledge on the role of oxidative stress and COX-derived prostanoids in the vascular alterations observed in hypertension, highlighting new findings indicating that these two pathways act in concert to induce vascular dysfunction.

scholarly journals Oxidative Stress and Autophagy in Cardiac Disease, Neurological Disorders, Aging and Cancer

2010 ◽  
Vol 3 (3) ◽  
pp. 168-177 ◽  
Author(s):  
Eric E. Essick ◽  
Flora Sam
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiac Disease ◽  
Neurological Disorders ◽  
Cell Stress ◽  
Nutrient Deprivation ◽  
Ros Production ◽  
Oxygen Species ◽  
Disease States ◽  
Cellular Components

Autophagy is a catalytic process of the bulk degradation of long-lived cellular components, ultimately resulting in lysosomal digestion within mature cytoplasmic compartments known as autophagolysosomes. Autophagy serves many functions in the cell, including maintaining cellular homeostasis, a means of cell survival during stress (e.g., nutrient deprivation or starvation) or conversely as a mechanism for cell death. Increased reactive oxygen species (ROS) production and the resulting oxidative cell stress that occurs in many disease states has been shown to induce autophagy. The following review focuses on the roles that autophagy plays in response to the ROS generated in several diseases.

Effects of Maternal Obesity and Gestational Diabetes Mellitus on the Placenta: Current Knowledge and Targets for Therapeutic Interventions

2020 ◽  
Vol 19 (2) ◽  
pp. 176-192
Author(s):  
Samantha Bedell ◽  
Janine Hutson ◽  
Barbra de Vrijer ◽  
Genevieve Eastabrook
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Maternal Obesity ◽  
Environmental Changes ◽  
Current Knowledge ◽  
Therapeutic Interventions ◽  
Placental Development ◽  
Exchange Site ◽  
And Function

: Obesity and gestational diabetes mellitus (GDM) are becoming more common among pregnant women worldwide and are individually associated with a number of placenta-mediated obstetric complications, including preeclampsia, macrosomia, intrauterine growth restriction and stillbirth. The placenta serves several functions throughout pregnancy and is the main exchange site for the transfer of nutrients and gas from mother to fetus. In pregnancies complicated by maternal obesity or GDM, the placenta is exposed to environmental changes, such as increased inflammation and oxidative stress, dyslipidemia, and altered hormone levels. These changes can affect placental development and function and lead to abnormal fetal growth and development as well as metabolic and cardiovascular abnormalities in the offspring. This review aims to summarize current knowledge on the effects of obesity and GDM on placental development and function. Understanding these processes is key in developing therapeutic interventions with the goal of mitigating these effects and preventing future cardiovascular and metabolic pathology in subsequent generations.

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