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Programmed Cell Death in Animal Development and Disease
Open accessAbstract
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, neurodegeneration, and cancer. Here, we provide a brief historical overview of the field and reflect on the regulation, roles, and modes of PCD during animal development. We also discuss the function and regulation of apoptotic proteins, including caspases, the key executioners of apoptosis, and review the nonlethal functions of these proteins in diverse developmental processes, such as 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.
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“On the one hand, RCD can occur in the absence of any exogenous environmental perturbation, hence operating as a built-in effector of physiological programs for development or tissue turnover [6, 18].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [6]
In the citing paper
“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 compartment, and oncosuppression [948–957].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [6]
In the citing paper
“Alternatively, these phagocytes may promote cell death to sculpt tissue structures and create functional circuits (Fuchs and Steller, 2011).”
From Developmental Heterogeneity of Microglia and Brain Myeloid Cells Revealed by Deep Single-Cell RNA Sequencing (2019) · cites this paper as Fuchs and Steller, 2011
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Metadata
- Authors
- Fuchs, Y., & Steller, H.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Steller, Hermann
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 147
- Issue
- 4
- Pages
- 742-758
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4511103
- OpenAlex
- W2042141743
- Cited by
- 1,915
- References
- 211
- Citations by year
- 2026: 79 · 2025: 122 · 2024: 188 · 2023: 166 · 2022: 153 · 2021: 204 · 2020: 146 · 2019: 129 · 2018: 135 · 2017: 106 · 2016: 129 · 2015: 123 · 2014: 91 · 2013: 85 · 2012: 55
- FWCI
- 6.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of General Medical Sciences (R01GM060124)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- programmed cell death, apoptosis, animal development, tissue homeostasis, caspases, cell differentiation, tissue remodeling, stem cells, cancer, neurodegeneration, immune disorders, wound healing, tissue regeneration
- MeSH terms
- Animals, Humans, Morphogenesis, Neoplasms, Stem Cells, Apoptosis, Neurodegenerative Diseases, Embryonic Development
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