Cell Death in Acute Organ Injury and Fibrosis

Dear Colleagues,

Tissue fibrosis is defined as excessive extracellular matrix deposition in any organ, including the lungs, liver, skin, kidneys, pancreas, and heart, which generally ends in organ failure. The process of fibrosis occurs due to tissue injury caused by different mechanisms, such as infection, trauma, metabolic disorders, wound, acute or chronic inflammation, autoimmune disorders, and cancer. Injury is followed by an abnormal tissue repair process characterized by the enhanced organ accumulation of fibroblasts and myofibroblasts that produce excessive extracellular matrix proteins. A variety of cells participate in the mechanism of fibrosis, including parenchymal epithelial cells, vascular endothelial cells, and cells from the innate or acquired immune systems that secrete factors that contribute to the recruitment and activation of extracellular matrix protein-producing fibroblasts. Importantly, during tissue injury and fibrosis, parenchymal cells undergo cell death, leading to the replacement of parenchymal cells by collagen-producing cells, further enhancing the fibrotic process. Cell death may occur by several mechanisms: apoptosis, necrosis, necroptosis, pyroptosis, ferroptosis, or autophagy. This Special Issue welcomes any study that evaluates the role of cell death in the pathogenesis of organ injury and fibrosis.

Prof. Dr. Esteban C. Gabazza
Dr. Taro Yasuma
Guest Editors

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