Macroautophagy is a cellular process that sequesters senescent or damaged organelles and proteins in autophagosomes for recycling their products. Autophagy is also involved in the removal of cells that have undergone classical apoptosis. Hence, autophagy can be generally considered as a protector of cells against various stressors and a cellular response to routine wear-and-tear. Paradoxically, autophagy may also be related to a form of non-apoptotic program cell death. Thus, autophagy can either protect cells or promote cell death, depending on the cellular and environmental context. Changes in autophagy are early events within the course of many degenerative diseases frequently associated with aging. Some of these modifications clearly precede the clinical diagnosis of these diseases and might mark the evolution from pre-clinical to overt diseases. Endocrine-metabolic diseases like type 2 diabetes, thyroid dysfunctions associated with the aging, non-alcoholic fatty liver disease and many forms of endocrine cancer are closely linked with disturbances into the autophagy flow. Even endothelial alterations related to these metabolic disturbances, including atherogenic processes, are associated to these modifications. Chronic complications of metabolic diseases are also linked to alterations in autophagy rates and flux. Sarcopenia and neurological age-associated degenerative diseases, such as Alzheimer disease, are pathophysiologically related to different forms of cell dysfunction linked to macroautophagy impairment. Imbalances in the antioxidant capacity within the cell result in oxidative stress-mediated injury. Selective autophagy mechanisms, as well as vesicular secretion and pathways related to senescence are relevant topics involved in the pathophysiology of these complex diseases. Some questions arise as natural consequence: Is autophagy a target for therapeutic intervention in these degenerative diseases? If affirmative, what is needed to do? What are the optimal autophagy rates and/or flux to be obtained at the critical tissues? Aligned with the answers to these and other related questions might help to the development of new therapies to take advantage of the potential cytoprotective effect of autophagy in chronic degenerative diseases as a potentially promising avenue of investigation.
We welcome authors to submit original research articles as well as review articles that will stimulate the continuing efforts to understand the impact of autophagy alterations on:
• Endocrine-metabolic diseases associated with aging, like type 2 diabetes, thyroid dysfunctions, non-alcoholic fatty liver disease and different forms of endocrine cancer
• Chronic complications of metabolic diseases: diabetes neuropathy and nephropathy, are also linked to alterations in autophagy rates and flux.
• Sarcopenia
• Neurological age-associated degenerative diseases, such as Alzheimer disease and other forms of dementia linked to metabolic disturbances
• Selective autophagy as a cell response to aging and metabolic, degenerative and tumoral diseases.
• Vesicular pathways and vesicular secretion in aging and metabolic, degenerative and tumoral diseases
• Autophagy and senescence in oncogenesis, tumor progression and metabolic diseases.
Macroautophagy is a cellular process that sequesters senescent or damaged organelles and proteins in autophagosomes for recycling their products. Autophagy is also involved in the removal of cells that have undergone classical apoptosis. Hence, autophagy can be generally considered as a protector of cells against various stressors and a cellular response to routine wear-and-tear. Paradoxically, autophagy may also be related to a form of non-apoptotic program cell death. Thus, autophagy can either protect cells or promote cell death, depending on the cellular and environmental context. Changes in autophagy are early events within the course of many degenerative diseases frequently associated with aging. Some of these modifications clearly precede the clinical diagnosis of these diseases and might mark the evolution from pre-clinical to overt diseases. Endocrine-metabolic diseases like type 2 diabetes, thyroid dysfunctions associated with the aging, non-alcoholic fatty liver disease and many forms of endocrine cancer are closely linked with disturbances into the autophagy flow. Even endothelial alterations related to these metabolic disturbances, including atherogenic processes, are associated to these modifications. Chronic complications of metabolic diseases are also linked to alterations in autophagy rates and flux. Sarcopenia and neurological age-associated degenerative diseases, such as Alzheimer disease, are pathophysiologically related to different forms of cell dysfunction linked to macroautophagy impairment. Imbalances in the antioxidant capacity within the cell result in oxidative stress-mediated injury. Selective autophagy mechanisms, as well as vesicular secretion and pathways related to senescence are relevant topics involved in the pathophysiology of these complex diseases. Some questions arise as natural consequence: Is autophagy a target for therapeutic intervention in these degenerative diseases? If affirmative, what is needed to do? What are the optimal autophagy rates and/or flux to be obtained at the critical tissues? Aligned with the answers to these and other related questions might help to the development of new therapies to take advantage of the potential cytoprotective effect of autophagy in chronic degenerative diseases as a potentially promising avenue of investigation.
We welcome authors to submit original research articles as well as review articles that will stimulate the continuing efforts to understand the impact of autophagy alterations on:
• Endocrine-metabolic diseases associated with aging, like type 2 diabetes, thyroid dysfunctions, non-alcoholic fatty liver disease and different forms of endocrine cancer
• Chronic complications of metabolic diseases: diabetes neuropathy and nephropathy, are also linked to alterations in autophagy rates and flux.
• Sarcopenia
• Neurological age-associated degenerative diseases, such as Alzheimer disease and other forms of dementia linked to metabolic disturbances
• Selective autophagy as a cell response to aging and metabolic, degenerative and tumoral diseases.
• Vesicular pathways and vesicular secretion in aging and metabolic, degenerative and tumoral diseases
• Autophagy and senescence in oncogenesis, tumor progression and metabolic diseases.
