Cover image of the article: Apoptosis: programmed cell death

Image Credit:J Inflamm Dis

Apoptosis: programmed cell death

Authors

Maryam Honardoost, Horyeh Soleimanjahi1, Farzad Rajaei
1Tarbiat Modarres University

Journal of Inflammatory Diseases:Vol. 17, issue 3; 48-57
Published online:Nov 01, 2013
Article type:issue_documents_importer
How to Cite:Honardoost M, Soleimanjahi H, Rajaei F. Apoptosis: programmed cell death. J Inflamm Dis. 2024;17(3):e155775. doi:

Abstract

  Apoptosis or programmed cell death is known as a conserved gene-directed mechanism for the specific elimination of unnecessary or unwanted cells from an organism and is involved in many immune system mechanisms and diseases . The main differences of this pathway with cell necrosis as two main pathways for elimination of unwanted cells are the absence of inflammation and the restricted effect on target cells. Apoptosis has an important role in biological processes such as normal development, tissue homeostasis, elimination of destroyed cells or virus infected cells and remove of self antigen-activated immune cells. A poptosis is important for regulation of cell growth and proliferation, development and body health and many autoimmune diseases, cancers and viral infections are the result of impaired or inhibited programmed cell death . Therefore the main objective of apoptosis research is to identify molecular components and regulatory mechanisms specially Bcl-2 and IAP family as the most important regulators of apoptosis and this information may lead to application of therapeutic agents that can modulate this process in the treatment of neurodegenerative disorders and proliferative diseases such as cancer.          

Copyright

© 2024, Journal of Inflammatory Diseases. This open-access article is available under the Creative Commons Attribution-NonCommercial 4.0 (CC BY-NC 4.0) International License (https://creativecommons.org/licenses/by-nc/4.0/), which allows for the copying and redistribution of the material only for noncommercial purposes, provided that the original work is properly cited.

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