ISSN: 2161-0681

Journal of Clinical & Experimental Pathology
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  • Mini Review   
  • J Clin Exp Pathol 2015, Vol 5(1): 205
  • DOI: 10.4172/2161-0681.1000205

Apoptosis-Biochemistry: A Mini Review

Madala Jayakiran*
Department of Oral Pathology, Mamata Dental College and Hospital, Khammam, India
*Corresponding Author : Madala Jayakiran, Department of Oral Pathology, Mamata Dental College and Hospital, Khammam, Andhra Pradesh, India, Tel: 91 9666057533, Email: jaikiran78@gmail.com

Received Date: Nov 25, 2014 / Accepted Date: Jan 07, 2015 / Published Date: Jan 15, 2015

Abstract

Apoptosis or programmed cell death is a normal component of the development and health of multicellular organisms. Homeostasis is maintained through a balance between cell proliferation and cell death. It is a process of controlled cellular death whereby the activation of specific death-signaling pathways leads to deletion of cells from tissue. The distinct morphological features of apoptosis are Cell shrinkage, Chromatin condensation, Membrane blebbing and formation of apoptotic bodies, which are phagocytosed by neighbouring macrophages without any inflammatory response. Derailment of apoptosis in regulation can lead to several diseases or ailments with either too much or too little apoptosis. Understanding the molecular mechanism of apoptosis including death genes, death signals, surface receptors and signal pathways will provide new insights in developing strategies to regulate cell survival/death. The current knowledge on the molecular events of apoptotic cell death and their significance in health and disease is reviewed.

Keywords: Apoptosis; Necrosis; Hemostasis; Caspases

Citation: Jayakiran M (2015) Apoptosis-Biochemistry: A Mini Review. J Clin Exp Pathol 5:205. Doi: 10.4172/2161-0681.1000205

Copyright: © 2015 Jayakiran M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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