Ferroptosis, apoptosis, necroptosis
1Institute of Experimental Medicine, Gebze-Kocaeli, Türkiye
2Republic of Türkiye Ministry of Agriculture And Forestry, Istanbul Food Control Laboratory Directorate, Istanbul, Türkiye
Keywords: Apoptosis, ferroptosis, necroptosis, programmed cell death.
Cell death processes developed to preserve tissue homeostasis and remove potentially hazardous or expired cells inside an organism, such as cells with damaged deoxyribonucleic acid that might cause illness. Cells have evolved various programmed cell death (PCD) pathways. Depending on the type of death signal in the cell, cell death occurs by activating the relevant death pathway and downstream components. Ferroptosis, apoptosis, and necroptosis, which are types of PCD, play an active role in many pathological and physiological processes, especially cancer, inflammation, neurodegenerative disorders, and immune system diseases. Although each pathway has its own set of stimuli and modulators, they do interact with one another. The downstream components of the relevant molecule involved in PCD and the molecules it interacts with enable the cell to choose the most ideal death pathway for the benefit of the cell. In this regard, identifying PCD pathways and their downstream components is critical for the creation of more effective disease treatments and medications, as well as for overcoming treatment resistance. This review article discussed the mechanisms of ferroptosis, apoptosis, and necroptosis as well as associated diseases.
Cite this article as: Açıkgöz S, Odabaşı M, Erbaş O. Ferroptosis, apoptosis, necroptosis. D J Tx Sci 2022;7(1-2):22-31.
Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.
All authors contributed equally to the article.
The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.
The authors received no financial support for the research and/or authorship of this article.