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Cell Aging --- Aging --- Cells --- Cellules --- physiology --- Periodicals. --- Vieillissement --- Périodiques --- physiology. --- Aging. --- Chemistry --- Health Sciences --- Life Sciences --- Biochemistry --- General and Others --- Biology --- Cellular Senescence --- Aging, Biological --- Biological Aging --- Senescence --- Cellular Aging --- Aging, Cell --- Cell Senescence --- Replicative Senescence --- Senescence, Cellular --- Senescence, Replicative --- Aging, Cellular --- Senescence, Cell --- ageing --- longevity --- lifespan --- apoptosis --- gerontology --- ageing --- Organisms --- Cytology --- Mutation Accumulation --- Cell Ageing --- Cellular Ageing --- Senescence-Associated Secretory Phenotype --- Ageing, Cell --- Ageing, Cellular --- Phenotype, Senescence-Associated Secretory --- Secretory Phenotype, Senescence-Associated --- Senescence Associated Secretory Phenotype --- Geriatrics --- gerontologie
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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
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Cell cycle --- Cell Cycle. --- DNA Damage. --- Cell Aging. --- Cell cycle. --- Celcyclus. --- Mitotic cycle --- Nuclear cycle (Cytology) --- Cellular Aging --- Aging, Cell --- Cell Senescence --- Replicative Senescence --- Senescence, Cellular --- Senescence, Replicative --- Aging, Cellular --- Cellular Senescence --- Senescence, Cell --- Injury, DNA --- DNA Injury --- Genotoxic Stress --- Stress, Genotoxic --- DNA Damages --- DNA Injuries --- Damage, DNA --- Damages, DNA --- Genotoxic Stresses --- Injuries, DNA --- Stresses, Genotoxic --- Cell Division Cycle --- Cell Cycles --- Cell Division Cycles --- Cycle, Cell --- Cycle, Cell Division --- Cycles, Cell --- Cycles, Cell Division --- Division Cycle, Cell --- Division Cycles, Cell --- Biological rhythms --- Cell Ageing --- Cellular Ageing --- Senescence-Associated Secretory Phenotype --- Cell Aging --- Ageing, Cell --- Ageing, Cellular --- Phenotype, Senescence-Associated Secretory --- Secretory Phenotype, Senescence-Associated --- Senescence Associated Secretory Phenotype --- Aging --- Mutation --- Pyrimidine Dimers --- Comet Assay --- DNA Repair Enzymes --- Cell Cycle Proteins --- Genes, cdc --- Cellular Senescence. --- Cell Cycle --- DNA Damage --- Cytologie --- Cellules --- Life Sciences --- Biology --- Cytology, Cell Biology --- DNA damage. --- Cells --- Cytology --- Cycle cellulaire --- Cycle cellulaire. --- ADN --- Aging. --- Lésions. --- Vieillissement. --- Biochemical genetics --- Mutation (Biology) --- Organisms --- Cytology. --- Cells. --- Cell biology --- Cellular biology
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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
Research & information: general --- Biology, life sciences --- 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 --- 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
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Recent biochemical studies indicate that calorie restriction (CR) is a widely accepted method for anti-aging intervention. CR and intermittent fasting (IF), which involves reduced calories but proper nutritional intake during specific periods, are interventions that can consistently promote health benefits, delay biological aging, and extend both average and maximal lifespan. Furthermore, CR can modulate age-related diseases such as Alzheimer’s disease, atherosclerosis, diabetes, obesity, cancer, and others. Advances in omics technologies have provided a technical breakthrough that enabled the investigation of DNA, RNA, proteins, and other cellular molecules and their comprehensive interactions in a biological context. Nowadays, it is possible to analyze and integrate biological processes that occur in aging systems at the molecular level using state-of-the-art techniques such as next-generation sequencing (NGS), proteomics, lipidomics, metabolomics, and epigenomics. Omics technology and systems gerontology provide predictive information on CR effects, molecular mechanisms, and pathways underlying the anti-aging actions of CR and IF. This Special Issue, “The effects of calorie restriction and intermittent fasting on health and disease”, focuses on the effects of calorie restriction and intermittent fasting on age-related inflammation, autophagy, metabolism, longevity, mitochondrial function, and age-related diseases.
Research & information: general --- Biology, life sciences --- Food & society --- calorie restriction diet --- body mass reduction --- insulin --- IGF-1 --- leptin --- adiponectin --- malnutrition --- heart impairment --- papillary muscle assay --- calcium transient proteins --- SERCA2a --- L-type calcium channel --- aging --- autophagy --- calorie restriction (CR) --- CR mimetic --- calorie restriction --- FoxO transcription factor --- sirtuin --- neuropeptide Y --- pleiotropy of CR genes --- senescence-associated secretory phenotype --- senoinflammation --- mimetics --- intermittent fasting --- fat mass --- insulin secretion --- pancreatic islet --- lifespan --- longevity --- fasting --- skin aging --- photoaging --- skin appendages --- caloric restriction --- fatty acid biosynthesis --- mitochondrial biogenesis --- adipocyte --- calorie restriction diet --- body mass reduction --- insulin --- IGF-1 --- leptin --- adiponectin --- malnutrition --- heart impairment --- papillary muscle assay --- calcium transient proteins --- SERCA2a --- L-type calcium channel --- aging --- autophagy --- calorie restriction (CR) --- CR mimetic --- calorie restriction --- FoxO transcription factor --- sirtuin --- neuropeptide Y --- pleiotropy of CR genes --- senescence-associated secretory phenotype --- senoinflammation --- mimetics --- intermittent fasting --- fat mass --- insulin secretion --- pancreatic islet --- lifespan --- longevity --- fasting --- skin aging --- photoaging --- skin appendages --- caloric restriction --- fatty acid biosynthesis --- mitochondrial biogenesis --- adipocyte
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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
Research & information: general --- Biology, life sciences --- 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
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Recent biochemical studies indicate that calorie restriction (CR) is a widely accepted method for anti-aging intervention. CR and intermittent fasting (IF), which involves reduced calories but proper nutritional intake during specific periods, are interventions that can consistently promote health benefits, delay biological aging, and extend both average and maximal lifespan. Furthermore, CR can modulate age-related diseases such as Alzheimer’s disease, atherosclerosis, diabetes, obesity, cancer, and others. Advances in omics technologies have provided a technical breakthrough that enabled the investigation of DNA, RNA, proteins, and other cellular molecules and their comprehensive interactions in a biological context. Nowadays, it is possible to analyze and integrate biological processes that occur in aging systems at the molecular level using state-of-the-art techniques such as next-generation sequencing (NGS), proteomics, lipidomics, metabolomics, and epigenomics. Omics technology and systems gerontology provide predictive information on CR effects, molecular mechanisms, and pathways underlying the anti-aging actions of CR and IF. This Special Issue, “The effects of calorie restriction and intermittent fasting on health and disease”, focuses on the effects of calorie restriction and intermittent fasting on age-related inflammation, autophagy, metabolism, longevity, mitochondrial function, and age-related diseases.
calorie restriction diet --- body mass reduction --- insulin --- IGF-1 --- leptin --- adiponectin --- malnutrition --- heart impairment --- papillary muscle assay --- calcium transient proteins --- SERCA2a --- L-type calcium channel --- aging --- autophagy --- calorie restriction (CR) --- CR mimetic --- calorie restriction --- FoxO transcription factor --- sirtuin --- neuropeptide Y --- pleiotropy of CR genes --- senescence-associated secretory phenotype --- senoinflammation --- mimetics --- intermittent fasting --- fat mass --- insulin secretion --- pancreatic islet --- lifespan --- longevity --- fasting --- skin aging --- photoaging --- skin appendages --- caloric restriction --- fatty acid biosynthesis --- mitochondrial biogenesis --- adipocyte --- n/a
Choose an application
Recent biochemical studies indicate that calorie restriction (CR) is a widely accepted method for anti-aging intervention. CR and intermittent fasting (IF), which involves reduced calories but proper nutritional intake during specific periods, are interventions that can consistently promote health benefits, delay biological aging, and extend both average and maximal lifespan. Furthermore, CR can modulate age-related diseases such as Alzheimer’s disease, atherosclerosis, diabetes, obesity, cancer, and others. Advances in omics technologies have provided a technical breakthrough that enabled the investigation of DNA, RNA, proteins, and other cellular molecules and their comprehensive interactions in a biological context. Nowadays, it is possible to analyze and integrate biological processes that occur in aging systems at the molecular level using state-of-the-art techniques such as next-generation sequencing (NGS), proteomics, lipidomics, metabolomics, and epigenomics. Omics technology and systems gerontology provide predictive information on CR effects, molecular mechanisms, and pathways underlying the anti-aging actions of CR and IF. This Special Issue, “The effects of calorie restriction and intermittent fasting on health and disease”, focuses on the effects of calorie restriction and intermittent fasting on age-related inflammation, autophagy, metabolism, longevity, mitochondrial function, and age-related diseases.
Research & information: general --- Biology, life sciences --- Food & society --- calorie restriction diet --- body mass reduction --- insulin --- IGF-1 --- leptin --- adiponectin --- malnutrition --- heart impairment --- papillary muscle assay --- calcium transient proteins --- SERCA2a --- L-type calcium channel --- aging --- autophagy --- calorie restriction (CR) --- CR mimetic --- calorie restriction --- FoxO transcription factor --- sirtuin --- neuropeptide Y --- pleiotropy of CR genes --- senescence-associated secretory phenotype --- senoinflammation --- mimetics --- intermittent fasting --- fat mass --- insulin secretion --- pancreatic islet --- lifespan --- longevity --- fasting --- skin aging --- photoaging --- skin appendages --- caloric restriction --- fatty acid biosynthesis --- mitochondrial biogenesis --- adipocyte --- n/a
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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
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