Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The problem of clinical pain management is complex and far-reaching, as it encompasses many different types of pain, such as arthritis, musculoskeletal conditions, neuropathic pain, and visceral pain. The analgesics market is growing and the driving forces are the aging population and need for better therapeutic benefits. There are various analgesic products that are available that can be administered by various routes, yet research is active in identifying new technologies for better drug targeting and novel targets to gain improved therapeutic efficiency. It is widely known that many of the well-established analgesic pathways are centrally based, involving spinal and supraspinal sites. However, pain can also be effectively controlled by peripheral pathways. For example, peripheral endogenous analgesia can be elicited by immune cells entering inflamed tissue and releasing opioid peptides that activate up-regulated opioid receptors on sensory nerve terminals. Such analgesic effects are particularly prominent in painful inflammatory conditions and avoid central opioid side effects. In this Research Topic of Frontiers, we would like to bring together experts in the field of pain at the physiological, pharmacological and pharmaceutical levels to discuss novel pain targets and new pain technologies. The goal of this workshop is to generate collaborative discussion on the future and direction of pain therapies. Manuscripts describing original research, methods, hypothesis and theory, and reviews are welcomed.

Pathology --- Medicine --- Health & Biological Sciences --- Pain --- Analgesics --- Targeted Drug Delivery --- novel strategies --- Therapeutic target

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Immunology --- STAT --- IRF --- innate immunity --- inflammation --- transcriptional regulation --- therapeutic target

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This book gathers a collection of review articles aiming to provide an update of the current knowledge on PD pathogenesis. It notably includes an overview of several key cellular dysfunctions underlying the etiology of Parkinson’s disease, including ER stress, mitophagy and alpha-synuclein-linked pathology.

Parkinson’s disease --- unfolded protein response --- reticulum endoplasmic --- genetics --- alpha-synuclein --- prion-like spreading --- cell-to-cell transfer --- neurodegeneration --- mitochondrial dysfunction --- PINK1 --- neurons --- astrocytes --- microglia --- α-synuclein --- exocytosis --- lipids --- membranes --- Parkinson disease --- SNARE complex --- synapse --- vesicle fusion --- therapeutic target --- protein quality control --- mitochondrial quality control --- ubiquitin --- alpha-syn --- mitophagy --- Parkin --- mito-Keima --- mito-QC --- mito-SRAI

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

MicroRNAs (miRNAs) are small noncoding RNAs that are 19–24 nucleotides in length, following maturation. Recent evidence has demonstrated their key role as post-transcriptional regulators of gene expression through the binding of specific sequences within target messenger RNA (mRNA). miRNAs are involved in the synthesis of a very large number of proteins, and it is speculated that they could regulate up to 30% of the human genome. They control virtually every cellular process and are essential for animal development, cell differentiation, and homeostasis. Altered miRNA expression has been linked to such pathological events as inflammatory, degenerative, or autoimmune processes and have been associated with several diseases, including cancer, cardiovascular diseases, diabetes mellitus, and rheumatic and neurological disorders. Recently, miRNAs have been found in many different biological fluids, and this observation suggests the potential of miRNAs as new candidate biomarkers for diagnosis, classification, prognosis, and responsiveness in the treatment of different pathological conditions. Furthermore, the development of therapeutic strategies that involve either restoring or repressing miRNAs expression and activity has attracted much attention. Significant progress has been made in the systems for delivery of miRNAs, even if substantial improvements in this area are still necessary. Although they have been extensively studied, a number of interesting questions regarding the physiological and pathological role of miRNAs have been postulated, and their potential diagnostic and therapeutic role remain yet unanswered. Reactive oxygen species (ROS) are free radical-containing oxygen molecules derived from cellular oxidative metabolism, including enzyme activities and mitochondrial respiration, and play a pivotal role in many cellular functions. Whereas ROS are essential for normal cellular processes, their aberrant production, or failure of the capacity to scavenge excessive ROS, induces an altered redox status with excessive synthesis of free radicals, leading to an imbalance in the redox environment of the cell. The loss of normal ROS levels causes lipid, protein, and DNA damage, which contribute to the development of various pathologies including neurological disorders, rheumatic and cardiovascular diseases, diabetes, and cancer. Increasing evidence highlights that there is crosstalk between miRNAs and components of redox signaling, even if this complex and the characteristics of mutual interaction need to be amply elucidated. Hence, both miRNAs and oxidative stress are involved in the multifactorial development and progression of acute and chronic diseases by influencing numerous signaling and metabolic pathways. The Special Issue entitled "Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology" of the International Journal of Molecular Sciences includes original articles and reviews that provide new insights into the interaction between miRNAs and oxidative stress under normal and pathological conditions which can assist in the development of new therapeutic strategies. Finally, I would like to thank all the authors for their excellent contribution. I hope this Special Issue will provide readers with updated knowledge about the role of miRNAs and oxidative stress in physiology and pathology.

Medicine --- miR-27a-5p --- acute myocardial infarction --- autophagy --- apoptosis --- hypoxia --- MicroRNA (miRNA) --- miR526b --- miR655 --- oxidative stress --- reactive oxygen species (ROS) --- superoxide (SO) --- Thioredoxin Reductase 1 (TXNRD1) --- breast cancer --- nucleic acid medicine --- pancreatic cancer --- clinical trial --- siRNA --- antisense oligonucleotide --- MicroRNA --- signal transduction --- therapeutic target --- miRNAs --- ROS --- noncoding RNA --- microRNA --- long noncoding RNA --- mitochondrial dysfunction --- nitrosative stress. exosome --- cross-talk --- systemic lupus erythematosus --- visfatin --- resistin --- osteoarthritis --- synovial fibroblasts --- synovitis --- NF-κB --- thyroid hormone --- liver cancer --- metabolism --- physiology --- ASH --- NAFLD --- NASH --- HCC --- HCV --- HBV --- endometriosis --- high-grade serous ovarian cancer --- endometriosis-associated ovarian cancer --- epithelial-to-mesenchymal transition --- chemoresistance --- antioxidants --- miRNA --- cancer --- diabetes --- beta cells --- microRNAs --- translation regulation --- neurodegeneration --- Alzheimer’s disease --- Parkinson’s disease --- Huntington’s disease --- ALS --- reactive oxygen species --- redox signaling --- therapeutic tolerance --- therapeutic resistance --- n/a --- Alzheimer's disease --- Parkinson's disease --- Huntington's disease

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.

Humanities --- Social interaction --- deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases