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    The role of programmed cell death in diabetic foot ulcers
    Juncheng Li et al
    Int Wound J. 2023 Sep 22
     
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    "Programmed cell death (PCD; sometimes referred to as cellular suicide[1]) is the death of a cell as a result of events inside of a cell, such as apoptosis or autophagy.[2][3] PCD is carried out in a biological process, which usually confers advantage during an organism's lifecycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. PCD serves fundamental functions during both plant and animal tissue development."

    Programmed cell death

    Death of a cell mediated by intracellular program, often as part of development

    Programmed cell death (PCD; sometimes referred to as cellular suicide[1]) is the death of a cell as a result of events inside of a cell, such as apoptosis or autophagy.[2][3] PCD is carried out in a biological process, which usually confers advantage during an organism's lifecycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. PCD serves fundamental functions during both plant and animal tissue development.

    Apoptosis and autophagy are both forms of programmed cell death.[4] Necrosis is the death of a cell caused by external factors such as trauma or infection and occurs in several different forms. Necrosis was long seen as a non-physiological process that occurs as a result of infection or injury,[4] but in the 2000s, a form of programmed necrosis, called necroptosis,[5] was recognized as an alternative form of programmed cell death. It is hypothesized that necroptosis can serve as a cell-death backup to apoptosis when the apoptosis signaling is blocked by endogenous or exogenous factors such as viruses or mutations. Most recently, other types of regulated necrosis have been discovered as well, which share several signaling events with necroptosis and apoptosis.[6]

    1. ^ Raff, M (12 November 1998). "Cell suicide for beginners". Nature. 396 (6707): 119–22. Bibcode:1998Natur.396..119R. doi:10.1038/24055. ISSN 0028-0836. PMID 9823889. S2CID 4341684.
    2. ^ Engelberg-Kulka H, Amitai S, Kolodkin-Gal I, Hazan R (2006). "Bacterial Programmed Cell Death and Multicellular Behavior in Bacteria". PLOS Genetics. 2 (10): e135. doi:10.1371/journal.pgen.0020135. PMC 1626106. PMID 17069462.
    3. ^ Green, Douglas (2011). Means To An End. New York: Cold Spring Harbor Laboratory Press. ISBN 978-0-87969-887-4.
    4. ^ a b Kierszenbaum, Abraham (2012). Histology and Cell Biology - An Introduction to Pathology. Philadelphia: ELSEVIER SAUNDERS.
    5. ^ Degterev, Alexei; Huang, Zhihong; Boyce, Michael; Li, Yaqiao; Jagtap, Prakash; Mizushima, Noboru; Cuny, Gregory D.; Mitchison, Timothy J.; Moskowitz, Michael A. (2005-07-01). "Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury". Nature Chemical Biology. 1 (2): 112–119. doi:10.1038/nchembio711. ISSN 1552-4450. PMID 16408008. S2CID 866321.
    6. ^ Vanden Berghe T, Linkermann A, Jouan-Lanhouet S, Walczak H, Vandenabeele P (2014). "Regulated necrosis: the expanding network of non-apoptotic cell death pathways". Nat Rev Mol Cell Biol. 15 (2): 135–147. doi:10.1038/nrm3737. PMID 24452471. S2CID 13919892.
     
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    Non-coding RNAs in diabetic foot ulcer- a focus on infected wounds
    Boquan Qin et al
    Diabetes Metab Res Rev. 2023 Oct 15
     
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    Advanced glycation end products regulate macrophage apoptosis and influence the healing of diabetic foot wound through miR-361-3p/CSF1R and PI3K/AKT pathway
    Yongzhi Jin et al
    Heliyon. 2024 Jan 17;10(2):e24598
     
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