Choose an application

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

CD4+ T lymphocytes play an essential role in host defense against bacterial, parasitic and viral infections. During infection, under the influence of intrinsic signals received through peptide-MHC/TCR interactions and extrinsic signals provided by pathogen-conditioned dendritic and other accessory cells, CD4+ T cells proliferate and differentiate into specialized T helper (Th) effectors, which produce distinct sets of cytokines tailored to combat a specific class of microbes. The concept of CD4+ T cell multi-functionality was developed after the seminal discovery of Th1 and Th2 cells nearly 30 years ago. Although the Th1/Th2 paradigm has successfully withstood the test of time, in the past decade additional Th subsets (Th17, Tfh, Th22, Th9) have been identified. Similarly, single cell analyses of cytokines and master transcriptional factors have revealed that, at the population level, CD4+ T cell responses are far more heterogeneous than initially anticipated. While some of the checkpoints in Th cell specification have been identified, recent studies of transcriptional and epigenetic regulation have uncovered a significant flexibility during the course CD4+ T lymphocyte polarization. In addition, Th cells expressing cytokines with counteracting functions, as a measure of self-regulation, display yet another level of diversity. Understanding the mechanisms that control the balance between stability vs. plasticity of Th effectors both at the time of initiation of immune response and during development of CD4 T cell memory is critical for the rational design of better vaccines and new immunotherapeutic strategies. This research topic will cover current views on Th cell development, with a focus on the mechanisms that govern differentiation, function and regulation of effector Th cells in the context of microbial infections.

Clinical Immunology --- Medicine --- Health & Biological Sciences --- Infection --- Dendritic Cells --- Cytokines --- Immunoregulation --- CD4 lymphocytes --- Memory --- long noncoding RNA --- Macrophages --- Metabolism --- Th1 Th2

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 --- 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

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)

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.

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)

This book provides important and updated information on current research devoted to urinary biomarkers. Urinary biomarkers are characteristics that can be objectively measured and evaluated as indicators of normal biological or pathogenic processes of pharmacological responses to therapeutic intervention.

Medicine --- poststreptococcal acute glomerulonephritis --- infection-related glomerulonephritis --- nephritis-associated plasmin receptor --- plasmin --- acute kidney injury --- renal biomarkers --- furosemide stress test --- functional assessment --- urine --- diabetic kidney disease --- kidney function --- proteomics --- mass spectrometry --- statistical clinical model --- machine learning --- acute tubulointerstitial nephritis --- immunology --- biomarkers --- chronic kidney disease --- differential diagnosis --- label-free quantification --- renal transplant --- extracellular vesicles --- acute rejection --- chronic rejection --- chronic allograft dysfunction --- calcineurin-inhibitor nephrotoxicity --- Polyomavirus associated nephropathy --- immunosuppression --- upper urinary tract obstruction --- kidney injury --- neutrophil gelatinase-associated lipocalin --- monocyte chemotactic protein-1 --- kidney injury molecule 1 --- cystatin C --- vanin-1 --- microRNA --- uromodulin --- kidney graft function --- biomarker --- kidney transplantation --- long noncoding RNA --- rejection --- microvascular injury --- urinary aminopeptidases --- arterial hypertension --- renal function --- urinary biomarkers --- markers of AKI --- cystatin-C --- NGAL --- KIM-1 --- exercise --- end-stage kidney disease (ESKD) --- cardiovascular disease --- epidemiology --- CKD --- macrophage subpopulation --- renal fibrosis --- trichostatin A --- kidney graft --- T-cell-mediated rejection --- antibody-mediated rejection --- diagnostic test accuracy --- gentamicin --- sepsis --- miRNA --- nephrotoxicity --- vancomycin --- poststreptococcal acute glomerulonephritis --- infection-related glomerulonephritis --- nephritis-associated plasmin receptor --- plasmin --- acute kidney injury --- renal biomarkers --- furosemide stress test --- functional assessment --- urine --- diabetic kidney disease --- kidney function --- proteomics --- mass spectrometry --- statistical clinical model --- machine learning --- acute tubulointerstitial nephritis --- immunology --- biomarkers --- chronic kidney disease --- differential diagnosis --- label-free quantification --- renal transplant --- extracellular vesicles --- acute rejection --- chronic rejection --- chronic allograft dysfunction --- calcineurin-inhibitor nephrotoxicity --- Polyomavirus associated nephropathy --- immunosuppression --- upper urinary tract obstruction --- kidney injury --- neutrophil gelatinase-associated lipocalin --- monocyte chemotactic protein-1 --- kidney injury molecule 1 --- cystatin C --- vanin-1 --- microRNA --- uromodulin --- kidney graft function --- biomarker --- kidney transplantation --- long noncoding RNA --- rejection --- microvascular injury --- urinary aminopeptidases --- arterial hypertension --- renal function --- urinary biomarkers --- markers of AKI --- cystatin-C --- NGAL --- KIM-1 --- exercise --- end-stage kidney disease (ESKD) --- cardiovascular disease --- epidemiology --- CKD --- macrophage subpopulation --- renal fibrosis --- trichostatin A --- kidney graft --- T-cell-mediated rejection --- antibody-mediated rejection --- diagnostic test accuracy --- gentamicin --- sepsis --- miRNA --- nephrotoxicity --- vancomycin