1,721,039 research outputs found
Coronavirus disease 2019 and non-alcoholic fatty liver disease
No full textThe coronavirus disease 2019 (COVID-19) pandemic may present with a broad range of clinical manifestations, from no or mild symptoms to severe disease. Patients with specific pre-existing comorbidities, such as obesity and type 2 diabetes, are at high risk of coming out with a critical form of COVID-19. Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and, because of its frequent association with metabolic alterations including obesity and type 2 diabetes, it has recently been re-named as metabolic-associated fatty liver disease (MAFLD). Several studies and systematic reviews pointed out the increased risk of severe COVID-19 in NAFLD/MAFLD patients. Even though dedicated mechanistic studies are missing, this higher probability may be justified by systemic low-grade chronic inflammation associated with immune dysregulation in NAFLD/MAFLD, which could trigger cytokine storm and hypercoagulable state after severe acute respiratory syndrome coronavirus 2 infection. This review focuses on the predisposing role of NAFLD/MAFLD in favoring severe COVID-19, discussing the available information on specific risk factors, clinical features, outcomes, and pathogenetic mechanisms
Cardiac visceral fat and cardiometabolic risk in the elderly
No full textAging is characterized by several changes in body mass composition with loss of muscle mass and increase in fat mass, particularly visceral fat. Visceral fat is represented mainly by abdominal and cardiac depots and it is directly related to chronic low-grade inflammation, insulin-resistance and metabolic syndrome. Unfavourable outcomes as cardiovascular death are also associated with the amount of visceral fat depots. In this scenario, the cardiac visceral fat seems to play an important role in increasing the cardiometabolic risk. This review aims to provide a literature revision about the role of cardiac visceral fat on cardiometabolic risk in elderly
Redox cell signaling and hepatic progenitor cells
No full textHepatic diseases are widespread in the world and organ transplantation is currently the only treatment for liver failure. New cell-based approaches have been considered, since stem cells may represent a possible source to treat liver diseases. Acute and chronic liver diseases are characterized by high production of reactive oxygen and nitrogen species, with consequent oxidative modifications of cellular macromolecules and alteration of signaling pathways, metabolism and cell cycle. Although considered harmful molecules, reactive species are involved in cell growth and differentiation processes, modulating the activity of transcription factors, which take part in stemness/proliferation. It is conceivable that redox balance may regulate the development of hepatic progenitor cells, function and survival in synchrony with metabolism during chronic liver diseases. This review aims to summarize diverse redox-sensitive signaling pathways involved in stem cell fate, highlighting the important role of hepatic progenitor cells as a possible source to treat end-stage liver disease for organ regeneration
Redox Homeostasis and Immune Alterations in Coronavirus Disease-19
No full textThe global Coronavirus Disease 2019 (COVID-19) pandemic is characterized by a wide variety of clinical features, from no or moderate symptoms to severe illness. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that first affects the respiratory tract. Other than being limited to lungs, SARS-CoV-2 may lead to a multisystem disease that can even be durable (long COVID). The clinical spectrum of COVID-19 depends on variability in the immune regulation. Indeed, disease progression is consequent to failure in the immune regulation, characterized by an intensification of the pro-inflammatory response. Disturbance of systemic and organ-related redox balance may be a further mechanism underlying variability in COVID-19 severity. Other than being determinant for SARS-CoV-2 entry and fusion to the host cell, reactive species and redox signaling are deeply involved in the immune response. This review sums up the present knowledge on the role of redox balance in the regulation of susceptibility to SARS-CoV-2 infection and related immune response, debating the effectiveness of antioxidant compounds in the management of COVID-19
Comparison of Catalytic Efficiency of Some Industrial Nanosized Titanium Dioxides in Heterogeneous Photodegradation by Chemometric Analysis
No full textRedox Control of the Immune Response in the Hepatic Progenitor Cell Niche
No full textThe liver commonly self-regenerates by a proliferation of mature cell types. Nevertheless, in case of severe or protracted damage, the organ renewal is mediated by the hepatic progenitor cells (HPCs), adult progenitors capable of differentiating toward the biliary and the hepatocyte lineages. This regeneration process is determined by the formation of a stereotypical niche surrounding the emerging progenitors. The organization of the HPC niche microenvironment is crucial to drive biliary or hepatocyte regeneration. Furthermore, this is the site of a complex immunological activity mediated by several immune and non-immune cells. Indeed, several cytokines produced by monocytes, macrophages and T-lymphocytes may promote the activation of HPCs in the niche. On the other side, HPCs may produce pro-inflammatory cytokines induced by liver inflammation. The inflamed liver is characterized by high generation of reactive oxygen and nitrogen species, which in turn lead to the oxidation of macromolecules and the alteration of signaling pathways. Reactive species and redox signaling are involved in both the immunological and the adult stem cell regeneration processes. It is then conceivable that redox balance may finely regulate the immune response in the HPC niche, modulating the regeneration process and the immune activity of HPCs. In this perspective article, we summarize the current knowledge on the role of reactive species in the regulation of hepatic immunity, suggesting future research directions for the study of redox signaling on the immunomodulatory properties of HPCs
The mediterranean diet slows down the progression of aging and helps to prevent the onset of frailty: A narrative review
Full text linkThe aging population is rapidly increasing all over the world. This results in significant implications for the planning and provision of health and social care. Aging is physiologically characterized by a decrease in lean mass, bone mineral density and, to a lesser extent, fat mass. The onset of sarcopenia leads to weakness and a further decrease in physical activity. An insufficient protein intake, which we often observe in patients of advanced age, certainly accelerates the progression of sarcopenia. In addition, many other factors (e.g., insulin resistance, impaired protein digestion and absorption of amino acids) reduce the stimulation of muscle protein synthesis in the elderly, even if the protein intake is adequate. Inadequate intake of foods can also cause micronutrient deficiencies that contribute to the development of frailty. We know that a healthy eating style in middle age predisposes to so-called “healthy and successful” aging, which is the condition of the absence of serious chronic diseases or of an important decline in cognitive or physical functions, or mental health. The Mediterranean diet is recognized to be a “healthy food” dietary pattern; high adherence to this dietary pattern is associated with a lower incidence of chronic diseases and lower physical impairment in old age. The aim of our review was to analyze observational studies (cohort and case–control studies) that investigated the effects of following a healthy diet, and especially the effect of adherence to a Mediterranean diet (MD), on the progression of aging and on onset of frailty
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