RT info:eu-repo/semantics/article
T1 The mechanisms of regulated cell death: Structural and functional proteomic pathways induced or inhibited by a specific protein—A narrative review
A1 Fernández Lázaro, Diego
A1 Sanz, Begoña
A1 Seco Calvo, Jesús
K1 Programmed cell death
K1 Cell death
K1 Células - Muerte
K1 Caspases
K1 Mitotic catastrophe
K1 Pyroptosis
K1 Parthanatos
K1 Nervous system - Degeneration
K1 Sistema nervioso - Degeneración
K1 Ferroptosis
K1 Entosis
K1 Proteomics
K1 Proteòmica
K1 Proteins
K1 Cell Biology
K1 2302.27 Proteínas
K1 2407 Biología Celular
AB Billions of cells die in us every hour, and our tissues do not shrink because there is a natural regulation where Cell Death (CD) is balanced with cell division. The process in which cells eliminate themselves in a controlled manner is called Programmed Cell Death (PCD). The PCD plays an important role during embryonic development, in maintaining homeostasis of the body’s tissues, and in the elimination of damaged cells, under a wide range of physiological and developmental stimuli. A multitude of protein mediators of PCD have been identified and signals have been found to utilize common pathways elucidating the proteins involved. This narrative review focuses on caspase-dependent and caspase-independent PCD pathways. Included are studies of caspase-dependent PCD such as Anoikis, Catastrophe Mitotic, Pyroptosis, Emperitosis, Parthanatos and Cornification, and Caspase-Independent PCD as Wallerian Degeneration, Ferroptosis, Paraptosis, Entosis, Methuosis, and Extracellular Trap Abnormal Condition (ETosis), as well as neutrophil extracellular trap abnormal condition (NETosis) and Eosinophil Extracellular Trap Abnormal Condition (EETosis). Understanding PCD from those reported in this review could shed substantial light on the processes of biological homeostasis. In addition, identifying specific proteins involved in these processes is mandatory to identify molecular biomarkers, as well as therapeutic targets. This knowledge could provide the ability to modulate the PCD response and could lead to new therapeutic interventions in a wide range of diseases.
PB MDPI
SN 2227-7382
YR 2024
FD 2024
LK https://uvadoc.uva.es/handle/10324/67281
UL https://uvadoc.uva.es/handle/10324/67281
LA eng
NO Proteomes,  2024, Vol. 12, Nº. 1, 3
NO Producción Científica
DS UVaDOC
RD 11-jul-2024