Programmed Cell Death in Animal Development and Disease
By Y. Fuchs, H. Steller. Cell, 2011
1,771 citations recorded by the source corpus.
Programmed Cell Death (PCD) plays a fundamental role in animal development and tissue homeostasis. Abnormal regulation of this process is associated with a wide variety of human diseases, including immunological and developmental disorders, neuro-degeneration, and cancer. Here, we provide a brief historical overview of the field and reflect on myriad functions carried out by PCD during development and explore how PCD is regulated. We also focus on the function and regulation of apoptotic proteins, including caspases, the key executioners of apoptosis, highlighting the non-lethal functions of these proteins in diverse developmental processes including cell differentiation and tissue remodeling. Finally, we explore a growing body of work about the connections between apoptosis, stem cells and cancer, focusing on how apoptotic cells release a variety of signals to communicate with their cellular environment, including factors that promote cell division, tissue regeneration, and wound healing.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/034cf5180d8692a0025099964ccad5566cc3ce61
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Citations in the corpus
- Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “Apoptosis, the programmed cell death, is finely regulated at gene level resulting in the orderly and efficient removal of damaged cells such as those occurring following DNA damage or during development [1].”
- Glutaminolysis and Transferrin Regulate Ferroptosis (2015, background): “In multicellular organisms, programmed cell death, particularly apoptosis, is frequently activated in a highly orchestrated manner to fulfill specific physiological functions (Budihardjo et al., 1999; Danial and Korsmeyer, 2004; Fuchs and Steller, 2011; Green and Kroemer, 2004; Thompson, 1995).”
- Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “Therefore, APP has been the subject of intense research as one possible cause for mitochondrial dysfunction in AD (Fuchs and Steller, 2011; Hirai et al., 2001).”
- Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis (2022, background): “During development, several structures that operate a transitory function are removed by PCD when they are no longer required [1,2].”
- Global Survey of Cell Death Mechanisms Reveals Metabolic Regulation of Ferroptosis (2016, background): “Viability of four engineered BJ cell lines treated with (a) CIL56 or (e) FIN56 for 48 hrs. mut: cells tumor-transformed due to HRASG12V overexpression, wt: isogenic cells without HRASG12V. b. Lipid ROS generation.”
- Programmed cell senescence during mammalian embryonic development. (2013, neutral): “…apoptosis also plays an important role during animal development, where it occurs in a well-defined manner in response to developmental cues, and it is classically referred to as developmentally programmed cell death (Conradt, 2009; Fuchs and Steller, 2011; Kourtis and Tavernarakis, 2007).”
- Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “One of the best-described mechanisms of programmed cell death is apoptosis, which is mediated through the activation of members of the caspase family of proteases (Fuchs and Steller, 2011; Kumar, 2007; Taylor et al., 2008).”
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Waves of cellular senescence (followed by RCD) appear to contribute to developmental embryogenesis (although in a dispensable manner) [6, 946, 947] as well as to multiple pathophysiological processes in the adult, including tissue repair and regeneration, immunity, preservation of the stem cell comp”
- Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012, background): “Cell death is crucial for normal development, homeostasis, and the prevention of hyperproliferative diseases such as cancer (Fuchs and Steller, 2011; Thompson, 1995).”