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Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

Medicine --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage

Choose an application

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

Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn’s disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- n/a --- Crohn's disease