Nowadays, silver nanoparticles (AgNPs) are the most widely used nanoparticles (NPs) in the industry due to their peculiar biocidal features. However, the use of these NPs still runs into limitations ...mainly because of the low efficiency of environmental friendly synthesis methods and lack of size standardization. When NPs are release in the environment, they can be transformed by oxidation, adsorption or aggregation. These modification shows a dual role in toxic response of AgNPs. The adsorption of natural organic matter from environment on AgNPs, for example, can decrease their toxicity. Otherwise oxidation occurred in the environment is also able to increase the release of toxic Ag+ from NPs. Thus, the current review proposes an integrated approach of AgNP synthetic methods using bacteria, fungi, and plants, AgNP cytotoxic and genotoxic effects as well as their potential therapeutic applications are also presented.
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•The AgNPs cytotoxicity can be used for therapeutic applications.•AgNPs released into the environment may react with various compounds found in aquatic organic matter•There are environmental friendly AgNP synthetic methods using bacteria, fungi, and plants.•The improvement of green synthesis methods will allow a better modeling of the AgNPs physicochemical characteristics.•The development of efficient green synthetic methods will contribute to potentiate AgNPs therapeutic effect.
The intestinal epithelium of fish is the major absorptive barrier for nutrients assisted by a large number of microbes. These are known as resident microbiota or gut microbiota, which has a symbiotic ...relationship with the host, playing key roles in pathogen protection, nutritional, endocrine, neural, and physiological functions. Dysbiosis is an impairment in the balance of the commensal communities forming the gut microbiota. This imbalance is caused by several factors with physiological consequences for the host and subsequent reduced growth and higher mortality rates. Therapeutic modulation strategies of the gut microbiota have been successfully used in higher vertebrate models; however, these procedures can also be adapted for their application to fish and other aquatic animals. Strategies such as probiotics, prebiotics, synbiotics, paraprobiotics, and postbiotics, as well as other emerging strategies, are discussed as potential therapeutic approaches for treating or avoiding dysbiosis in fish.
•Gut microbiota dysbiosis affects the physiological performance of fish.•Therapeutic measures used in higher vertebrates to alleviate dysbiosis can be applied to fish.•Probiotics, prebiotics, synbiotics, paraprobiotics, and postbiotics are the most promising strategies.•Phytogenics, phage therapy, and bacterial consortia transplantation emerge as promising therapeutic alternatives.
Cancer is a multistep disease driven by the activation of specific oncogenic pathways concomitantly with the loss of function of tumor suppressor genes that act as sentinels to control physiological ...growth. The conservation of most of these signaling pathways in
, and the ability to easily manipulate them genetically, has made the fruit fly a useful model organism to study cancer biology. In this review we outline the basic mechanisms and signaling pathways conserved between humans and flies responsible of inducing uncontrolled growth and cancer development. Second, we describe classic and novel
models used to study different cancers, with the objective to discuss their strengths and limitations on their use to identify signals driving growth cell autonomously and within organs, drug discovery and for therapeutic approaches.
A BSTRACT Cystic fibrosis (CF) is a life-threatening genetic disorder caused by mutations in the CFTR gene. This leads to a defective protein that impairs chloride transport, resulting in thick mucus ...buildup and chronic inflammation in the airways. The review discusses current and future therapeutic approaches for CFTR dysfunction and airway dysbiosis in the era of personalized medicine. Personalized medicine has revolutionized CF treatment with the advent of CFTR modulator therapies that target specific genetic mutations. These therapies have significantly improved patient outcomes, slowing disease progression, and enhancing quality of life. It also highlights the growing recognition of the airway microbiome’s role in CF pathogenesis and discusses strategies to modulate the microbiome to further improve patient outcomes. This review discusses various therapeutic approaches for cystic fibrosis (CFTR) mutations, including adenovirus gene treatments, nonviral vectors, CRISPR/cas9 methods, RNA replacement, antisense-oligonucleotide-mediated DNA-based therapies, and cell-based therapies. It also introduces airway dysbiosis with CF and how microbes influence the lungs. The review highlights the importance of understanding the cellular and molecular causes of CF and the development of personalized medicine to improve quality of life and health outcomes.
Type 2 diabetes (T2D) and its target organ injuries cause distressing impacts on personal health and put an enormous burden on the healthcare system, and increasing attention has been paid to ...T2D-associated cognitive dysfunction (TDACD). TDACD is characterized by cognitive dysfunction, delayed executive ability, and impeded information-processing speed. Brain imaging data suggest that extensive brain regions are affected in patients with T2D. Based on current findings, a wide spectrum of non-specific neurodegenerative mechanisms that partially overlap with the mechanisms of neurodegenerative diseases is hypothesized to be associated with TDACD. However, it remains unclear whether TDACD is a consequence of T2D or a complication that co-occurs with T2D. Theoretically, anti-diabetes methods are promising neuromodulatory approaches to reduce brain injury in patients with T2D. In this review, we summarize potential mechanisms underlying TDACD and promising neurotropic effects of anti-diabetes methods and some neuroprotective natural compounds. Constructing screening or diagnostic tools and developing targeted treatment and preventive strategies would be expected to reduce the burden of TDACD.
•TDACD is a highly prevalent and age-dependent complication of T2D.•Extensive but nonspecific changes in the brain underlie TDACD.•Improved healthy lifestyle and GLP-1RAs might mitigate TDACD.
Nuclear factor-κB (NF-κB) is a transcription factor that plays a crucial role in various biological processes, including immune response, inflammation, cell growth and survival, and development. ...NF-κB is critical for human health, and aberrant NF-κB activation contributes to development of various autoimmune, inflammatory and malignant disorders including rheumatoid arthritis, atherosclerosis, inflammatory bowel diseases, multiple sclerosis and malignant tumors. Thus, inhibiting NF-κB signaling has potential therapeutic applications in cancer and inflammatory diseases.
Post-stroke depression (PSD) is a prevalent neuropsychiatric condition that affects approximately one-third of stroke survivors, leading to impaired rehabilitation and reduced quality of life. ...Despite its significant impact, the precise mechanisms underlying PSD remain incompletely understood. Emerging evidence suggests that inflammation may play a pivotal role in its pathogenesis. Notably, recent studies have highlighted the involvement of the pro-inflammatory cytokine interleukin-18 (IL-18) in PSD. Elevated levels of IL-18 following stroke have been observed, indicating its potential contribution to the propagation of inflammation, disruption of neurotransmitter balance, and neuronal damage. IL-18 may also serve as a valuable biomarker for predicting the risk of PSD. Moreover, dysregulation of IL-18 signaling has emerged as a critical factor in the development of PSD. Therefore, modulating IL-18 expression holds promise as a strategy to prevent the progression of PSD. This review provided a comprehensive summary of the current evidence elucidating the diverse immunological and pathological mechanisms of IL-18 in PSD. We also assessed therapeutic strategies that target IL-18 signaling for the management and treatment of PSD. By elucidating the multifaceted role of IL-18 in PSD, this review provides insights into potential therapeutic avenues for improving the outcomes and well-being of individuals affected by PSD.
Neurodegenerative disorders (NDs) are expected to pose a significant challenge for both medicine and public health in the upcoming years due to global demographic changes. NDs are mainly represented ...by degeneration/loss of neurons, which is primarily accountable for severe mental illness. This neuronal degeneration leads to many neuropsychiatric problems and permanent disability in an individual. Moreover, the tight junction of the brain, blood-brain barrier (BBB)has a protective feature, functioning as a biological barrier that can prevent medicines, toxins, and foreign substances from entering the brain. However, delivering any medicinal agent to the brain in NDs (i.e., Multiple sclerosis, Alzheimer's, Parkinson's, etc.) is enormously challenging. There are many approved therapies to address NDs, but most of them only help treat the associated manifestations. The available therapies have failed to control the progression of NDs due to certain factors, i.e., BBB and drug-associated undesirable effects. NDs have extremely complex pathology, with many pathogenic mechanisms involved in the initiation and progression; thereby, a limited survival rate has been observed in ND patients. Hence, understanding the exact mechanism behind NDs is crucial to developing alternative approaches for improving ND patients' survival rates. Thus, the present review sheds light on different cellular mechanisms involved in NDs and novel therapeutic approaches with their clinical relevance, which will assist researchers in developing alternate strategies to address the limitations of conventional ND therapies. The current work offers the scope into the near future to improve the therapeutic approach of NDs.
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•Advancement in nanotechnology is a boon for cellular repair in mental disorders.•Molecular mechanisms in NDs could augment mental illness therapies and research.•Clinical insights may improve understanding of limits and benefits of NDs therapies.
Rheumatoid arthritis (RA) is a common, chronic, systemic autoimmune disease, and its clinical features are the proliferation of joint synovial tissue, the formation of pannus and the destruction of ...cartilage. The global incidence of RA is about 1%, and it is more common in women. The basic feature of RA is the body's immune system disorders, in which autoreactive CD4
T cells, pathogenic B cells, M1 macrophages, inflammatory cytokines, chemokines and autoantibodies abnormally increase in the body of RA patients B cell depletion therapy has well proved the important role of B cells in the pathogenesis of RA, and the treatment of RA with B cells as a target has also been paid more and more attention. Although the inflammatory indicators in RA patients receiving B-cell depletion therapy have been significantly improved, the risk of infection and cancer has also increased, which suggests that we need to deplete pathogenic B cells instead of all B cells. However, at present we cannot distinguish between pathogenic B cells and protective B cells in RA patients. In this review, we explore fresh perspectives upon the roles of B cells in the occurrence, development and treatment of RA.
Diabetic neuropathy is a heterogeneous group of disorders with extremely complex pathophysiology and affects both somatic and autonomic components of the nervous system. Neuropathy is the most common ...chronic complication of diabetes mellitus. Metabolic disruptions in the peripheral nervous system, including altered protein kinase C activity, and increased polyol pathway activity in neurons and Schwann cells resulting from hyperglycemia plays a key role in the development of diabetic neuropathy. These pathways are related to the metabolic and/or redox state of the cell and are the major source of damage. Activation of these metabolic pathways leads to oxidative stress, which is a mediator of hyperglycemia induced cell injury and a unifying theme for all mechanisms of diabetic neuropathy. The therapeutic intervention of these metabolic pathways is capable of ameliorating diabetic neuropathy but therapeutics which target one particular mechanism may have a limited success. Available therapeutic approaches are based upon the agents that modulate pathogenetic mechanisms (glycemic control) and relieve the symptoms of diabetic neuropathy. This review emphasizes the pathogenesis, presently available therapeutic approaches and future directions for the management of diabetic neuropathy.
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