Tissues usually mend after being harmed. The acknowledgment that harm has occurred is required for cellular responses to heal. Apoptotic cell death is often triggered by the cell’s surroundings. In fact, when cells are overworked, persistent cellular stress can trigger homeostatic repair systems or cause them to die. Apoptosis causes parenchymal cell death in the kidney during acute and chronic renal damage, although it does not cause an inflammatory response. Inflammation, on the other hand, can cause necrosis, which is distinguished from apoptosis by the loss of plasma membrane integrity, resulting in the release of unprocessed intracellular content, including cellular organelles, which are immunogenic proteins. Depending on the intensity of the insult, the relative contribution of apoptosis and necrosis to injury varies. Immunologically silent apoptosis or immunogenic necrosis can cause regulated cell death. Recent advancements have improved The concept of controlled necrosis is the most groundbreaking. Necroptosis, ferroptosis, pyroptosis, parhanatos, mitochondria permeability transition regulated necrosis, and NETosis are some of the regulated necrosis modes that have been described. Mitochondria, which are well-known for their canonical roles in cellular respiration and oxidative phosphorylation, are also recognised as key contributors in the cell death pathway, playing a key role in detecting and integrating environmental signals to trigger adaptive and compensatory responses in cells. As a result, mitochondrial damage and malfunction have been identified as a pathogenic event in a number of disorders, including Kidney disease can be both chronic and acute. As a result, we explore the several modalities of cell death in kidney injury, emphasising converging cell death pathways and demonstrating that a combination therapy targeting multiple cell-death pathways may lead to novel therapeutic prospects.
Author (s) Details
Giovanna Priante
Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine – DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Lisa Gianesello
Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine – DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Monica Ceol
Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine – DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Associate Professor Dorella Del Prete
Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine – DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
Franca Anglani
Kidney Histomorphology and Molecular Biology Laboratory, Clinical Nephrology, Department of Medicine – DIMED, University of Padua, via Giustiniani 2, 35128 Padova, Italy.
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