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Radiobiology of Cell Death
1951 - 1970
Radiobiology becomes the dominant framework for cell death research, focusing on dose–survival dynamics, repair of X-ray–induced damage, and chromosomal effects across mammalian cells with methods to quantify damage and repair. Programmed cell death is studied as a regulated developmental process modulated by endocrine signals and pharmacologic factors. Hematologic death paradigms emphasize red blood cell turnover and immune-mediated destruction, while hepatic cell death and necrosis under toxic or ischemic stress reveal liver-specific vulnerability; mitochondrial dysfunction accompanies necrosis, linking subcellular integrity to cell viability.
• Radiation biology emerges as the dominant framework for cell death research in this era, emphasizing dose–survival dynamics, repair of X-ray damage, and chromosomal effects across mammalian cells with methods to quantify damage and repair [1], [5], [7], [13], [16].
• Programmed cell death is studied as a regulated developmental process with endocrine modulation and pharmacologic influence, illustrated by silkmoth muscle degeneration and hormone/drug effects on cell fate [8], [12].
• Red blood cell death and turnover, including immune-mediated destruction, autohemolysis, and viability/dye-based assessment methods, reflect hematologic death paradigms and diagnostic approaches [4], [6], [10], [17], [18], [19].
• Hepatic cell death and necrosis under toxic, ischemic, and stress-related conditions, with chemical/physical/ultrastructural characterization of liver cell demise [3], [9], [11].
• Mitochondrial dysfunction and ultrastructural alterations accompany necrosis in liver cells, highlighting subcellular pathways that connect mitochondrial integrity to cell viability [9], [11].
Caspase-Bcl-2 Axis
1971 - 1995
Extrinsic-Intrinsic Crosstalk
1996 - 2006
Autophagy-Regulated Cell Death
2007 - 2013
Integrated Regulated Cell Death
2014 - 2023