1,721,117 research outputs found
Role of Scavenger Receptor B1 (SR-B1) in Improving Food Benefits for Human Health
No full textScavenger receptor class B member 1 (SR-B1) is a multiligand receptor with a broad range of functions spanning from the uptake of cholesteryl esters from high-density lipoproteins (HDLs) and transport of micronutrients such as fat-soluble vitamins and carotenoids across cell membranes
to roles in tumor progression, pathogen recognition, and inflammatory responses. As a target of exposome factors such as environmental stressors and unhealthy lifestyle choices, as well as aging, dysregulated expression and activity of SR-B1 can negatively impact human health. Intriguingly, not only is SR-B1 a major determinant of nutrient homeostasis and, hence, metabolic
health status, but these same nutrients and some phytochemicals have also
demonstrated their ability to modulate SR-B1. Therefore, an integrated
approach that, taking into account human health, nutrition, and food tech-
nology sciences, aims to produce foods with health-promoting effects should
take advantage of the multifaceted properties of SR-B1. Improved func-
tional foods and novel nanoparticle-based delivery systems, rich in nutrients
and phytochemicals, with precise targeting to SR-B1 in specific tissues or
structures could represent a strategic advance to improve human health and
promote well-being
Mitochondrial involvement in the development and progression of diseases
No full textMitochondria arose evolutionally through a fateful endosymbiosis more than 1.45 billion years ago. While the functions of mitochondria are fairly well characterized under normal physiological conditions, there are important aspects of mitochondrial involvement in several pathological settings that still remain poorly understood/investigated. In this context, this Special Issue was designed to better clarify the mitochondrial role in the progression and development of specific pa- thologies, including neurological and rare/orphan diseases. Mitochon- drial involvement in these disorders has been attributed to the ability of these organelles to trigger deadly machineries such as apoptosis, ne- crosis, and autophagy that will then affect tissues and organs [1,2]. More recently, it has been shown that ferroptosis and inflammasome activa- tion are also associated with atypical mitochondrial function [3–5]. Therefore, the aim of this special issue was to bring together the state of the art on the still unexplained and unexplored role of mitochondria in orphan and neurological disorders. A total of 19 manuscripts were accepted for publication and most of them related to the link between mitochondria and neurological conditions
Oxidative-Stress-Sensitive microRNAs in UV-Promoted Development of Melanoma
No full textSIMPLE SUMMARY: Exposure to ultraviolet (UV) rays from the sun is one of the most important modifiable risk factors for skin cancer. Melanoma is the most life-threatening type of skin cancer. UV-induced DNA damage and oxidative stress represent two main mechanisms that, directly and indirectly, contribute to melanomagenesis. In addition, an interplay of abnormally expressed microRNAs (miRNAs) and redox imbalance is a hallmark in several cancers, including melanoma. UV radiation can be the central hub between these two cellular aberrations, as it is able to stimulate both. Here, to gain new mechanistic insights into melanomagenesis and identify new therapeutic targets for the prevention and treatment of melanoma, we report current evidence suggesting a complex interaction between UV-promoted deregulation of redox-sensitive miRNAs and known signal-transduction pathways underlying malignant transformation of melanocytes to melanoma. ABSTRACT: Melanoma is the most aggressive and life-threatening form of skin cancer. Key molecular events underlying the melanocytic transformation into malignant melanoma mainly involve gene mutations in which exposure to ultraviolet (UV) radiation plays a prominent role. However, several aspects of UV-induced melanomagenesis remain to be explored. Interestingly, redox-mediated signaling and perturbed microRNA (miRNA) profiles appear to be interconnected contributing factors able to act synergistically in melanoma initiation and progression. Since UV radiation can promote both redox imbalance and miRNA dysregulation, a harmful crosstalk between these two key cellular networks, with UV as central hub among them, is likely to occur in skin tissue. Therefore, decoding the complex circuits that orchestrate the interaction of UV exposure, oxidative stress, and dysregulated miRNA profiling can provide a deep understanding of the molecular basis of the melanomagenesis process. Furthermore, these mechanistic insights into the reciprocal regulation between these systems could have relevant implications for future therapeutic approaches aimed at counteracting UV-induced redox and miRNome imbalances for the prevention and treatment of malignant melanoma. In this review, we illustrate current information on the intricate connection between UV-induced dysregulation of redox-sensitive miRNAs and well-known signaling pathways involved in the malignant transformation of normal melanocytes to malignant melanoma
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Evidences of altered Redox Homeostasis in Trichothiodystrophy
No full textTrichothiodystrophy (TTD) is a rare hereditary disease whose prominent feature is brittle hair. Additional clinical signs are physical and neurodevelopmental abnormalities and in about half of the cases hypersensitivity to UV radiation. Although the mutations involved in this condition have been characterized, the correlation between the molecular defects and the plethora of clinical symptoms is not well understood. Recently, the presence of a redox imbalance in TTD has been suggested although no clear evidence has been reported on this aspect
Omega-3 nutritional intervention as therapeutic co-adjuvant approach to improve Rett syndrome clinical and biochemical features
No full textOmega-3 polyunsaturated fatty acids (PUFAs) have well-demonstrated beneficial effects as anti-inflammatory/immune-modulatory molecules and regulate multiple biological functions (i.e., blood pressure, maternal/child health, correct neurological development)
Redox regulation of cutaneous AMPs by ozone in tensioned skin models
No full textOzone-induced inflammation has been linked to the development of skin ailments including atopic dermatitis, acne vulgaris, eczema and psoriasis, mainly through a redox-inflammatory pathway. While ozone cannot penetrate the cutaneous layers, it is able to damage the skin through oxinflammatory reactions in the epidermis that lead to the generation of lipid-peroxides, aldehydes, and H2O2. When the production of these bioactive oxidative molecules overwhelms the cutaneous redox defenses, cutaneous damage incurs. Antimicrobial peptides (AMPs) are effector molecules that regulate a variety of cutaneous immune responses. Increased AMPs levels have also been detected in active lesions of inflammatory skin diseases. Our previous research has shown that exposure to either ozone induced the expression of cutaneous AMPs (LL-37, beta-defensin 2, and beta-defensin 3) levels in ex vivo skin explants, corroborating the hypothesis that ozone exposure might worsen inflammatory skin conditions via AMPs de-regulation. In the present work, to further assess the cutaneous AMPs responses in a more physiological setting, skin models cultured under physiological tension (TenBio) were expose to ozone. As a proof of concept, cutaneous models were pre-treated with a variety of redox inhibitors (catalase, deferoxamine (DFO) and VAS2870 (VAS)) before ozone exposure to better understand the involvement of a redox signaling. Our data demonstrates that even in the most realistic cutaneous ex vivo model, ozone induces LL-37, hBD2, and hBD3 protein levels through a redox mechanism. This study lays the basis to uncover the mechanisms of ozone dysregulation of cutaneous AMPs, a fundamental step to understanding the development/worsening of pollution-linked inflammatory skin conditions
Inflammation in Neurological Disorders: The Thin Boundary between Brain and Periphery
No full textSignificance: Accumulating evidence suggests that inflammation is a major contributor in the pathogenesis of several highly prevalent, but also rare, neurological diseases. In particular, the neurodegenerative processes of Alzheimer's disease (AD), vascular dementia (VAD), Parkinson's disease (PD), and multiple sclerosis (MS) are fueled by neuroinflammation, which, in turn, is accompanied by a parallel systemic immune dysregulation. This cross-talk between periphery and the brain becomes substantial when the blood-brain barrier loses its integrity, as often occurs in the course of these diseases. It has been hypothesized that the perpetual bidirectional flux of inflammatory mediators is not a mere "static"collateral effect of the neurodegeneration, but represents a proactive phenomenon sparking and driving the neuropathological processes. However, the upstream/downstream relationship between inflammatory events and neurological pathology is still unclear. Recent Advances: Solid recent evidence clearly suggests that metabolic factors, systemic infections, Microbiota dysbiosis, and oxidative stress are implicated, although to a different extent, in the development in brain diseases. Critical Issues: Here, we reviewed the most solid published evidence supporting the implication of the axis systemic inflammation-neuroinflammation-neurodegeneration in the pathogenesis of AD, VAD, PD, and MS, highlighting the possible cause of the putative downstream component of the axis. Future Directions: Reaching a definitive clinical/epidemiological appreciation of the etiopathogenic significance of the connection between peripheral and brain inflammation in neurologic disorders is pivotal since it could open novel therapeutic avenues for these diseases
Ox-inflammasome involvement inneuroinflammation
No full textNeuroinflammation plays a crucial role in the onset and the progression of several neuropathologies, from neurodegenerative disorders to migraine, from Rett syndrome to post-COVID 19 neurological manifestations. Inflammasomes are cytosolic multiprotein complexes of the innate immune system that fuel inflammation. They have been under study for the last twenty years and more recently their involvement in neuro-related conditions has been of great interest as possible therapeutic target. The role of oxidative stress in inflammasome activation has been described, however the exact way of action of specific endogenous and exogenous oxidants needs to be better clarified. In this review, we provide the current knowledge on the involvement of inflammasome in the main neuropathologies, emphasizing the importance to further clarify the role of oxidative stress in its activation including the role of mitochondria in inflammasome-induced neuroinflammation
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