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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2 --- n/a
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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2 --- n/a
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Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response. This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.
Medicine --- Oncology --- sonodynamic therapy --- carbon doped titanium dioxide --- sonosensitizers --- ultrasound --- cancer treatment --- breast cancer treatment --- radiotherapy --- hematological malignancies --- oxidative stress --- lymphoma --- leukemia --- multiple myeloma --- apoptosis --- mitochondria --- ultraviolet-C (UVC) --- withanolide --- combined treatment --- oral cancer --- DNA damage --- cancer therapy --- immune system --- Hypericum perforatum --- hyperforin --- reactive oxygen species --- pH regulation --- tumor prevention --- tumor therapy --- cancerogenesis --- inflammatory signaling --- natural compounds --- pancreatic cancer --- antitumor agents --- coordination polymers --- bioinorganic chemistry --- cold atmospheric plasma --- reactive oxygen and nitrogen species --- nitrite --- cancer stem cells --- chemoresistance --- glutathione --- lipid peroxidation --- ZEB-1 --- GPX4 --- ferroptosis --- HO-1 --- Nrf2 --- cancer progression --- patients --- therapy --- prognosis --- biomarker --- Eprenetapopt --- Erastin --- glutathione (GSH) --- SLC7A11 --- iron --- NRF2
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Alveolar epithelial cells (AECs) of the lung are important contributors to pulmonary immune functions and to pulmonary development and alveolar repair mechanisms following lung injury. AECI, together with the capillary endothelium, form the extremely thin barrier between alveolar air and blood. AECII produce and metabolize the surface-tension lowering and immune-modulating surfactant and are the progentiors of AECI. A great variety of processes rely on their normal functioning, including maintenance of the alveolar barrier; innate immune defense; and processes of differentiation, senescence, apoptosis, and autophagy. The wide range of AEC functions is nicely reflected by the diversity of topics addressed by the four review and eight original articles contained in this Special Issue of the International Journal of Molecular Sciences. Beyond the broad spectrum of topics, the authors of this issue also made use of an impressive variety of analytical methods, thus further illustrating the fascinating diversity of aspects related to AEC biology.
Research & information: general --- Biology, life sciences --- JAM-A --- P2X7 receptor --- mouse lung --- alveolar epithelium --- bleomycin-induced lung injury --- GSK-3β --- dietary sugar --- hyperglycemia --- lung mechanics --- alveolar septal composition --- physical activity --- extracellular matrix remodeling --- high-altitude pulmonary edema --- acute mountain sickness --- oxygen diffusion limitation --- surfactant protein B --- atelectrauma --- alveolar fluid --- acinar micromechanics --- acute lung injury --- autophagy --- lysosome --- lysosomal membrane permeability --- mitochondria --- pneumocyte --- microRNA-21 --- alveolar micromechanics --- structural remodeling --- inflammatory signaling --- lung --- alveolus --- type 1 alveolar epithelial cell --- type 2 alveolar epithelial cell --- focused ion beam scanning electron microscopy --- 3D reconstruction --- carbon dioxide --- hypercapnia --- Na,K-ATPase --- endoplasmic reticulum --- sodium transport --- protein oxidation --- alveolar epithelial cells --- pulmonary fibrosis --- epithelial cell dysfunction --- stem cell exhaustion --- pneumonia --- necrotizing --- regeneration --- model --- bovine --- chlamydia --- alveoli --- air-blood barrier --- epithelium --- air-liquid interface --- alveolar lining layer --- glycocalyx --- surfactant --- lung injury --- lung regeneration
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Alveolar epithelial cells (AECs) of the lung are important contributors to pulmonary immune functions and to pulmonary development and alveolar repair mechanisms following lung injury. AECI, together with the capillary endothelium, form the extremely thin barrier between alveolar air and blood. AECII produce and metabolize the surface-tension lowering and immune-modulating surfactant and are the progentiors of AECI. A great variety of processes rely on their normal functioning, including maintenance of the alveolar barrier; innate immune defense; and processes of differentiation, senescence, apoptosis, and autophagy. The wide range of AEC functions is nicely reflected by the diversity of topics addressed by the four review and eight original articles contained in this Special Issue of the International Journal of Molecular Sciences. Beyond the broad spectrum of topics, the authors of this issue also made use of an impressive variety of analytical methods, thus further illustrating the fascinating diversity of aspects related to AEC biology.
JAM-A --- P2X7 receptor --- mouse lung --- alveolar epithelium --- bleomycin-induced lung injury --- GSK-3β --- dietary sugar --- hyperglycemia --- lung mechanics --- alveolar septal composition --- physical activity --- extracellular matrix remodeling --- high-altitude pulmonary edema --- acute mountain sickness --- oxygen diffusion limitation --- surfactant protein B --- atelectrauma --- alveolar fluid --- acinar micromechanics --- acute lung injury --- autophagy --- lysosome --- lysosomal membrane permeability --- mitochondria --- pneumocyte --- microRNA-21 --- alveolar micromechanics --- structural remodeling --- inflammatory signaling --- lung --- alveolus --- type 1 alveolar epithelial cell --- type 2 alveolar epithelial cell --- focused ion beam scanning electron microscopy --- 3D reconstruction --- carbon dioxide --- hypercapnia --- Na,K-ATPase --- endoplasmic reticulum --- sodium transport --- protein oxidation --- alveolar epithelial cells --- pulmonary fibrosis --- epithelial cell dysfunction --- stem cell exhaustion --- pneumonia --- necrotizing --- regeneration --- model --- bovine --- chlamydia --- alveoli --- air-blood barrier --- epithelium --- air-liquid interface --- alveolar lining layer --- glycocalyx --- surfactant --- lung injury --- lung regeneration
Choose an application
Alveolar epithelial cells (AECs) of the lung are important contributors to pulmonary immune functions and to pulmonary development and alveolar repair mechanisms following lung injury. AECI, together with the capillary endothelium, form the extremely thin barrier between alveolar air and blood. AECII produce and metabolize the surface-tension lowering and immune-modulating surfactant and are the progentiors of AECI. A great variety of processes rely on their normal functioning, including maintenance of the alveolar barrier; innate immune defense; and processes of differentiation, senescence, apoptosis, and autophagy. The wide range of AEC functions is nicely reflected by the diversity of topics addressed by the four review and eight original articles contained in this Special Issue of the International Journal of Molecular Sciences. Beyond the broad spectrum of topics, the authors of this issue also made use of an impressive variety of analytical methods, thus further illustrating the fascinating diversity of aspects related to AEC biology.
Research & information: general --- Biology, life sciences --- JAM-A --- P2X7 receptor --- mouse lung --- alveolar epithelium --- bleomycin-induced lung injury --- GSK-3β --- dietary sugar --- hyperglycemia --- lung mechanics --- alveolar septal composition --- physical activity --- extracellular matrix remodeling --- high-altitude pulmonary edema --- acute mountain sickness --- oxygen diffusion limitation --- surfactant protein B --- atelectrauma --- alveolar fluid --- acinar micromechanics --- acute lung injury --- autophagy --- lysosome --- lysosomal membrane permeability --- mitochondria --- pneumocyte --- microRNA-21 --- alveolar micromechanics --- structural remodeling --- inflammatory signaling --- lung --- alveolus --- type 1 alveolar epithelial cell --- type 2 alveolar epithelial cell --- focused ion beam scanning electron microscopy --- 3D reconstruction --- carbon dioxide --- hypercapnia --- Na,K-ATPase --- endoplasmic reticulum --- sodium transport --- protein oxidation --- alveolar epithelial cells --- pulmonary fibrosis --- epithelial cell dysfunction --- stem cell exhaustion --- pneumonia --- necrotizing --- regeneration --- model --- bovine --- chlamydia --- alveoli --- air-blood barrier --- epithelium --- air-liquid interface --- alveolar lining layer --- glycocalyx --- surfactant --- lung injury --- lung regeneration
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