Choose an application

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

Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor

γH2AX --- Alzheimer’s disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3 --- n/a --- Alzheimer's disease

Choose an application

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

Cell death. --- Cellules --- Mort. --- Cell degeneration --- Cells --- Death (Biology) --- Cell Death. --- Apoptosis. --- Therapeutics. --- Therapy --- Treatment --- Therapeutic --- Therapies --- Treatments --- Disease --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Death, Cell --- Cellular Senescence --- therapy

Choose an application

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

Oxidative Stress --- Cell aging --- Oxidative stress --- Cells --- Stress oxydatif --- Cellules --- Periodicals --- Aging --- Périodiques --- Vieillissement --- Oxidative Stress. --- Cell Aging. --- Oxidative stress. --- Aging. --- Life Sciences --- Biology --- oxidative stress --- cell aging --- Cell Aging --- Oxidation-reduction reaction --- Stress (Physiology) --- Organisms --- Cytology --- Cell Ageing --- Cellular Ageing --- Cellular Aging --- Senescence-Associated Secretory Phenotype --- Aging, Cell --- Cell Senescence --- Replicative Senescence --- Senescence, Cellular --- Senescence, Replicative --- Ageing, Cell --- Ageing, Cellular --- Aging, Cellular --- Phenotype, Senescence-Associated Secretory --- Secretory Phenotype, Senescence-Associated --- Senescence Associated Secretory Phenotype --- Senescence, Cell --- Stress, Oxidative --- Oxidative Stresses --- Stresses, Oxidative --- Nitrosative Stress --- Antioxidants --- Reactive Oxygen Species --- Cellular Senescence --- Cellular Senescence. --- Periodicals. --- Anti-oxidative Stress --- Antioxidative Stress --- DNA Oxidative Damage --- Nitro-Oxidative Stress --- Oxidative Cleavage --- Oxidative DNA Damage --- Oxidative Damage --- Oxidative Injury --- Oxidative Nitrative Stress --- Oxidative Stress Injury --- Oxidative and Nitrosative Stress --- Anti oxidative Stress --- Anti-oxidative Stresses --- Antioxidative Stresses --- Cleavage, Oxidative --- DNA Damage, Oxidative --- DNA Oxidative Damages --- Damage, DNA Oxidative --- Damage, Oxidative --- Damage, Oxidative DNA --- Injury, Oxidative --- Injury, Oxidative Stress --- Nitrative Stress, Oxidative --- Nitro Oxidative Stress --- Nitro-Oxidative Stresses --- Oxidative Cleavages --- Oxidative DNA Damages --- Oxidative Damage, DNA --- Oxidative Damages --- Oxidative Injuries --- Oxidative Nitrative Stresses --- Oxidative Stress Injuries --- Stress Injury, Oxidative --- Stress, Anti-oxidative --- Stress, Antioxidative --- Stress, Nitro-Oxidative --- Stress, Oxidative Nitrative --- Stresses, Nitro-Oxidative --- Histology. Cytology

Choose an application

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

This text is designed to provide conceptual outlines and detailed procedures for basic and advanced studies of cell death by apoptosis. Chapters on the recognition of apoptosis as distinguished from necrosis and nonspecific cell DNA damage, are followed by a systematic examination of the established and the principal novel methodologies utilized by some leading laboratories conducting research on apoptosis. The organization is on the lines of signalling for apoptosis, the apoptotic cascade, and the execution of apoptosis. A wide variety of procedures are provided which will enable the reader to participate in cutting-edge research.

Cell Death --- Cell Physiological Processes --- Cell Physiological Phenomena --- Phenomena and Processes --- Apoptosis --- Biology --- Health & Biological Sciences --- Cytology --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Cell Physiological Phenomenon --- Cell Physiological Process --- Physiology, Cell --- Cell Physiology --- Phenomena, Cell Physiological --- Phenomenon, Cell Physiological --- Physiological Process, Cell --- Physiological Processes, Cell --- Process, Cell Physiological --- Processes, Cell Physiological --- Cells --- Death, Cell --- Cellular Senescence --- physiology

Choose an application

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

Vision is the most important sense in higher mammals. The retina is the first step in visual processing and the window to the brain. It is not surprising that problems arising in the retina lead to moderate to severe visual impairments. We offer here a collection of reviews as well as original papers dealing with various aspects of retinal function as well as dysfunction. New approaches in retinal research are described, such as the expression and localization of the endocannabinoid system in the normal retina and the role of cannabinoid receptors that could offer new avenues of research in the development of potential treatments for retinal diseases. Moreover, new insights are offered in advancing knowledge towards the prevention and cure of visual pathologies, mainly AMD, RP, and diabetic retinopathy.

eye --- retina --- development --- vascularization --- hypoxia --- autophagy --- programmed cell death --- cellular senescence --- retinogenesis --- altricial bird species --- precocial bird species --- senescence-associated galactosidase activity --- diabetes mellitus --- retinopathy --- microvascular --- complication --- optical coherence tomography --- angiography --- black --- African-American --- systemic disease --- biomarker --- retinal degenerative diseases --- mesenchymal stem cells --- stem cell therapy --- experimental models --- clinical trials --- AMD --- age-related macular degeneration --- trichostatin A (TSA) --- HDAC --- histone deacetylase --- vascular endothelial growth factor (VEGF) --- retinal degeneration --- endoplasmic reticulum --- stress response --- unfolded protein response --- GRP78 --- retinal glial cell --- diabetic retinopathy --- zebrafish --- neurovascular unit --- microvascular complications and dysfunction --- metabolism --- motor protein --- myosin 1C --- photoreceptor --- rhodopsin --- outer segments --- visual function --- macroglia --- astrocytes --- Müller cells --- optic nerve crush --- retinal ganglion cells --- spinal cord injury --- signal transducer and activator of transcription 3 --- epidermal growth factor --- Drp1 --- apoptosis --- mitochondria --- microglia --- neurodegeneration --- multiple sclerosis --- retinal microglia --- microglia morphotype --- light damage --- functional analysis --- early detection --- remodeling --- lactate --- GPR81 --- HCAR1 --- growth cone --- dLGN --- axon --- 3,5-DHBA --- kallikrein-kinin system --- kinin receptors --- GFAP --- osteopontin --- retinal detachment --- diabetes --- antioxidants --- bioenergetics --- respiration --- ATP --- glucagon-like peptide-1 --- exendin-4 --- catalase --- immunohistochemistry --- electron microscopy --- Charles Bonnet syndrome --- EEG --- visual hallucination --- resting state --- high-fat diet --- gut microbiome --- gut-retina axis --- RNA sequencing --- germ-free mice --- complement cascade --- angiogenesis --- retinal inflammation --- AII amacrine cell --- Prox1 --- parvalbumin --- gap junction --- eccentricity --- ON/OFF asymmetry --- arterioles --- betulinic acid --- ischemia-reperfusion injury --- reactive oxygen species --- retinal vessels --- retinal fluorescence imaging --- amyloid --- cognitive decline --- Alzheimer’s disease --- optic neuritis --- oxidative stress --- neuroprotection --- fingolimod --- iPSC-RPE --- retinal pigment epithelium --- immunodeficient RCS rat --- ultrathin parylene --- retinal transplantation --- CD4+CD25+ --- inflammation --- iPSC --- typical cannabinoid receptors --- atypical cannabinoid receptors --- electroretinography --- monkeys --- visual system --- eye inflammation --- lipopolysaccharide --- natural bioactive extracts --- Ac2-26 --- FPR receptor --- inflammatory mediators --- retinal light injury --- LED screen --- optical filter --- retinal protection --- regeneration --- progenitor cell --- hyperglycemia --- photoreceptors --- neurod --- Notch --- n/a --- Müller cells --- Alzheimer's disease